Peri-Mucositis and Peri-Implantitis Diagnosis, Classifcation, Etiologies, and Therapies










1142
41
Peri-Mucositis and
Peri-Implantitis Diagnosis,
Classication, Etiologies,
and Therapies
JON B. SUZUKI AND KEVIN R. SUZUKI
I
mplant dentistry has evolved into an evidence-based,
clinical science with well-documented research to validate
previously unsupported clinical practice procedures. Sig-
nificant efforts that focus on the biology and biomechanics of
implant dentistry have helped to develop and refine clinical
techniques based on peer-reviewed findings. However, despite
improved and predictable clinical successes in implantol-
ogy, peri-implant diseases have been diagnosed with increas-
ing incidence. The evolution of research and understanding
of biologic concepts in implant dentistry and implant rescue
has caused many areas of debate and controversy. Innovative
theories have been developed that have resulted in technique
modifications. Science has spurred implant dentistry to new
pinnacles of success, which is highly based upon essential
principles of periodontal regeneration.
e tremendous expansion of knowledge in implant dentistry
has created new ideas and terminology that is redened based on
new applications to implant dentistry. In many instances new
research may contradict established paradigms. It may be chal-
lenging for clinicians to select correct protocols, procedures,
armamentarium, and techniques. As materials and techniques
are further investigated, dogma may undergo criticism and con-
troversy. Experienced clinicians consistently introduce and rene
techniques and instruments to maintain clinical excellence as
technology and research advance.
One area of expansion of knowledge and views relates to
the maintenance of dental implants. Early research explored
techniques and instruments that were current for the methods
and materials of that era. Although many of those implants
are still in function in patients today, research and advances in
technology have given us newer materials, implant design, and
protocols to maintain dental implant health.
An understanding of the mucoepithelial implant attachment
is essential before commencing maintenance procedures. Contro-
versies and parameters for probing and crestal bone loss are impor-
tant for clinicians to recognize. ere are anatomic and histologic
dierences between the attachment apparatus of teeth compared
with implants that are osseointegrated. e bacterial plaque bio-
lm on these implant-tissue attachments may be signicant to
clinical success.
When the clinician understands the parameters of implants
and teeth, specic maintenance plans may be established for the
patient to minimize the possibility of developing peri-implant dis-
ease. Clinicians should inform patients of expectations and out-
comes during treatment, and demonstrate oral hygiene options
appropriate during each stage. Patients need to recognize the
importance of maintenance protocols, and clinicians should assess
compliance to home care routines. Patients also should be com-
petent to perform home maintenance. ese strategies would cer-
tainly minimize risks for peri-implant disease and implant failures.
As the acceptance of and demand for dental implants increase,
the need to understand the importance of maintenance as it relates
to long-term implant success also increases. e role of the dental
hygienist in implant maintenance and care as well as diagnosing
peri-implant disease is increasing and becoming more dened.
Implants and associated prostheses are much dierent from nat-
ural teeth and may require adjunctive procedures and instruments
for professional and patient care. Complications may arise when
clinicians fail to comprehend these dierences, because they may
adversely impact the implant’s outcome, increasing the morbidity
of treatment. e techniques and protocols used must be eective
at removing biolms and accretions, and procedures performed by
patients and clinicians should avoid damage to the components of
the implant, abutment, restoration, and associated tissue.
Establishment and maintenance of the soft tissue seal around
the transmucosal portion of the implant enhances the success of
an implant. is barrier is fundamentally a result of appropriate
wound healing and connection of epithelial attachments. e
maintenance of healthy peri-implant tissues contributes to implant
success and minimizes peri-implant disease. In addition, tissues
free of inammation and a biolm-controlled implant sulcus will
support the patient’s general and oral health.

1143
CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies
Peri-implant Disease
One important, but often neglected, component of comprehen-
sive dental implant treatment is the postprosthetic evaluation and
treatment of peri-implant issues. ere are many conicting opin-
ions and controversies on the diagnosis and treatment of these
complications. Failure to eectively and promptly diagnose and
treat peri-implant disease with dental implants leads to an increase
in implant and prosthetic failure.
Dental professionals are initially trained to have a rm under-
standing of the disease processes associated with the natural denti-
tion. A variety of tests, indices, and radiographic signs are used to
determine the health of a natural tooth. Dental implants and their
related prostheses have fundamentally dierent relationships to
the oral environment than teeth, and these dierences necessitate
a change in diagnostic protocol for the determination of health.
Failure to understand these processes may lead to undiagnosed
disease states and potential morbidity of the implant system.
e implant clinician must have a strong understanding of the
anatomic and histologic dierences between natural dentition and
the dental implant as they pertain to periodontal structures. By
having this foundation, the clinician may appreciate these neces-
sary dierences and will be better equipped to eectively diagnose
peri-implant disease processes. With the increase in the number
of dental implants being placed each year, a resultant increase in
the incidence of peri-implant disease has been seen. Two condi-
tions of peri-implant disease are peri-implant mucositis and peri-
implantitis.
1
e 6th European Workshop on Periodontology in
2008 concluded that peri-implant diseases are infectious in nature
and are dened by “changes in the level of crestal bone, presence of
bleeding on probing, and/or suppuration; with or without deep-
ening of the peri-implant pockets.
2
In dierentiation between these two peri-implant conditions,
both have been shown to be localized around implants and dem-
onstrate features similar to adult chronic periodontal disease.
3
ese conditions may be analogous to gingivitis (peri-mucositis)
and periodontitis (peri-implantitis). However, biologic dierences
exist between the natural teeth and implants. Basically, peri-
implant tissues are more susceptible to infections, due to dier-
ences in soft tissue attachment and biolms that may advance to
the alveolar-implant complex (see discussion in Chapter 42).
4
Gingivitis is a bacteria-induced inammation involving the
region of the marginal gingiva above the crest of bone and adjacent
to a natural tooth. e most common forms are associated with
plaque and may be classied as: (1) acute necrotizing, (2) ulcerative,
(3) hormonal, (4) drug induced, or (5) spontaneously occurring.
5
ese categories may also relate to the gingival tissues around an
implant.
6,7
e classication of gingivitis and periodontitis has cur-
rently been updated by the American Academy of Periodontology.
8
e bacteria responsible for gingivitis around a tooth may
aect the epithelial attachment, without loss of connective tissue
attachment. Because the connective tissue attachment of a tooth
extends an average of 1.07 mm above the crestal bone, at least 1
mm of protective barrier above the bone is present. In contrast,
no connective tissue attachment zone exists around an implant
because there is an absence of connective bers that extend into
the implant surface. erefore no connective tissue barrier exists
to protect the crestal bone around an implant.
9
Periodontitis around teeth is characterized by apical movement
of junctional epithelium and periodontal attachment, coupled
with loss of alveolar bone. Bacteria are thought to be responsible
by stimulating the bodys immune response, which results in an
overall resorptive eect on the periodontal attachment appara-
tus. e American Academy of Periodontology (2018) recognizes
stages of periodontitis: stage 1, stage 2, stage 3, and stage 4. For-
mer specic subtypes
10
for each category such as adult chronic
periodontitis, rapidly progressive periodontitis, localized juvenile,
and prepubertal periodontitis are now encompassed within stage
1, stage 2, and stage 3 of periodontitis.
In contrast with teeth, early crestal bone loss around an implant
body prosthetically may not always be caused by pathogens. In
many cases, the associated bone loss may result from stress fac-
tors too great for the immature, incompletely mineralized bone-
implant interface or an extension of the biologic width onto a
smooth metal crest module.
11
erefore, an implant may exhibit
early crestal bone loss with a dierent mechanism or cause, com-
pared with natural teeth. However, bacteria in some cases may be
the primary factor, because anaerobic bacteria have been observed
in the microgap between the implant and the abutment or in the
sulcus of implants. is is especially evident when sulcus depths
are greater than 5 mm (Box 41.1).
12
A systematic review
13
high-
lights potential etiologies of early crestal bone loss around recently
osteointegrated implants.
In summary, periodontal disease that develops around dental
implants has been classied into two separate entities: peri-implant
mucositis and peri-implantitis. Peri-implant mucositis is dened as a
reversible inammatory reaction in the peri-implant tissues surround-
ing an implant. Peri-implantitis is dened as an inammatory reac-
tion, with loss of supporting bone around an implant (Fig. 41.1).
The Role of Biofilm in Peri-Implant Disease
e oral biolm originates from bacteria and saliva, which result
in sticky masses of bacteria with a polysaccharide matrix that accu-
mulate on hard and soft surfaces in the oral cavity. e bacterial
and biolm formation may adhere to any implant surfaces in the
oral cavity and have been reported to result in pocket formation
and loss of the supporting bone.
14-16
Di Giulio etal.
17
determined
that biolm is one of the major causes of implant failure. e
Consensus of the 7th European Workshop on Periodontology
stated that peri-implant infections are always caused by plaque
and its by-products (i.e., biolm).
18
e role of biolms has been heavily studied and has been
reported to be responsible for approximately 65% of peri-implant
diseases.
19
After exposure of the implant surface to the oral cav-
ity, a pellicle is formed in less than 30 minutes.
20
e pellicle is
derived from the saliva, various bacteria present in the oral cavity,
and also host tissue products. After formation of the pellicle, bac-
terial attachment occurs by cell-to-cell adhesion on the implant
surface.
21
Most bacteria use biolm as the primary method of
Shallow
• Gram-positivefacultativecocci,rods
• Gram-negativeanaerobiccocci,rods
• Motilerods
• Spirochetes
• Black-pigmentedbacteroides
• Fusobacterium
Deep
• Vibriosorganisms
BOX
41.1
Common Bacteria Associated With
Pocket Depths

1144
PART VIII Dental Implant Maintenance
growth, because they facilitate nutrient exchange and prevent
competing microorganisms.
22
Studies have shown the process of
biolm colonization is the same on teeth as with dental implants.
23
erefore the most ideal solution to prevent microbial infec-
tions is to decrease the colonization of bacteria on implant sur-
faces. Unfortunately, many characteristics (e.g., material, surface
roughness) of prosthetic and implant surfaces directly aect the
bacterial adhesion and biolm formation.
24
For reversal of the peri-implant disease process, the biolm
must be removed with mechanical debridement or chemical oblit-
eration. If not removed, mature plaque will form. It has been
shown that bacteria will migrate from teeth to implants and from
implant to implant. Similar to teeth, clinical ndings of failing
implants include inammation, pocket formation, and progres-
sive bone loss.
25
e microorganisms may initiate an inammatory release of
cytokines that will enhance accumulation of neutrophils to the
implant lesion. is process will continue to attract more leuko-
cytes and continue to facilitate more peri-implant tissue damage
and inammation.
26,27
If the inammation progresses, it will lead
to peri-implantitis, with the characteristic feature of bone loss
around the implant. If left untreated, stromal tissue cells may
also propagate, leading to an increase in inltrates of proinam-
matory cells that promotes further tissue breakdown,
28-30
which
may eventually lead to loss of osseointegration, implant mobility,
and ultimately implant failure.
31-33
In addition to the results of a
systematic review, there is evidence that the pathogens Prevotella
intermedia, Campylobacter rectus, Aggregatibacter actinomycetem-
comitans, and Treponema denticola have been implicated in the
pathogenesis of peri-implantitis.
34,35
Current chemotherapeutics cannot penetrate thick biolm,
because rough surfaces have been found to hold more biolm
than smooth surfaces.
36
Bacterial deposits produce exotoxins and
lipopolysaccharides (endotoxins) that inhibit broblast and osteo-
blastic growth, and thus prevent proximal regeneration onto the
implant surface. Although it is impossible to guarantee 100% ste-
rility of exposed implant surfaces, the body is capable of removing
small amounts of bacterial deposit via host defense mechanisms.
37
Carefully removing macrodeposits of plaque biolm and irri-
gating with antimicrobial solution is generally sucient to allow
a favorable environment for new attachment formation. It is rec-
ommended that patients complete a full-mouth debridement to
reduce bacterial colonies, including plaque biolms on exposed
implant surfaces (Box 41.2).
Peri-implant Mucositis
Peri-implant mucositis is an inammatory condition of the soft tis-
sue surrounding an implant, which is similar to gingivitis around
natural teeth. In both animal and human studies, peri-implant
mucositis has been shown clinically and histologically to be com-
parable to gingivitis around natural teeth.
184
is has been dened
A B
C D
Fig. . (A) Spongiotic gingivitis exhibiting erythematous marginal tissue with cyanotic tissue. (B) Peri-
odontitis: mandibular anterior exhibiting severe horizontal bone loss. (C) Peri-mucositis: erythematous buc-
cal gingiva with associated bleeding around implant crown. (D) Peri-implantitis: significant bone loss with
erythematous tissue with significant plaque accumulation. (From Suzuki JB, Misch CE. Periodontal and
maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implan-
tology. St. Louis, MO: Elsevier; 2018.)

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CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies
Bacteria
Prevotella intermedia
Porphyromonas gingivalis
Aggregatibacter actinomycetemcomitans
Tannerella forsythia (formerly Bacteroides forsythus)
Treponema denticola
Prevotella nigrescens
Fusobacterium nucleatum
Etiology
• PoorOralHygiene
• PoorCompliancewithSupportiveProcedures
• PoorProsthesisDesign
• PoorFitofProsthesis
• Non-idealImplantPosition
• LackofNon-KeratinizedPeri-ImplantMucosa
• RetainedCement
BOX
41.2
Bacteria and Etiology of Peri-Implant
Mucositis
AB
C
Fig. . Peri-mucositis. (A) Bleeding on probing without bone loss with a diagnosis of peri-mucositis.
(B) Inflammation on the buccal aspect of the mandibular first molar implant. (C) Maxillary overdenture causing
peri-mucositis and fungal infections.
implant level.
39
Clinically, bleeding on peri-implant probing with
mucositis may be present without suppuration. If peri-mucositis
is allowed to progress, peri-implantitis may result, which includes
loss of bone and possible loss of osseointegration, similar to loss of
attachment and bone with periodontitis. e relationship between
plaque accumulation and peri-implant mucosal inammation has
been proven through numerous studies (Fig. 41.2).
40-42
Etiology
Most cases of peri-implant mucositis are due to poor oral hygiene,
inability to clean the implant or prosthesis, nonideal implant
position, poor t of the prosthesis, and retained cement. Poorly
placed implants or overcontoured prostheses may lead to diculty
or inability to properly clean the implants (Fig. 41.3). In addition,
peri-implant mucositis may also be caused by titanium alloy hyper-
sensitivity. Most dental implants today are covered by a titanium
dioxide layer that gives the implant a high surface energy that
facilitates the interaction between the host tissues and the dental
implant. When the implant becomes exposed to the oral environ-
ment, a lower surface energy may provoke a type IV hypersensitiv-
ity reaction that may contribute to peri-implant mucositis.
43
Prevention
Because of the high prevalence of peri-implant mucositis, it is
imperative that the clinician be able to assess the risk prole of
each patient and integrate these considerations when treatment
as a reversible condition with no loss of attachment or bone loss.
e prevalence rate of peri-implant mucositis (bleeding on prob-
ing and no loss of bone) in systemic reviews has been shown to
be approximately 30% of implants and 47 % of patients.
38
How-
ever, other studies have reported the incidence to be as high as
80% of patients and 50 % of implants observed. Ferreira etal.
reported a prevalence of 64.6% at the patient level and 62.6% at

1146
PART VIII Dental Implant Maintenance
planning is initiated. A consensus report by the Academy of Peri-
odontology has shown risk factors to include poor oral hygiene,
history of periodontal disease, smoking, retained cement, and
occlusal disharmonies. erefore, a comprehensive medical his-
tory should be evaluated for any risk factors and the patient should
be informed of possible associated complications.
Tobacco smoking leads to the end product of nicotine and nor-
nicotine that increases cytokine levels and reactive oxygen species.
Increased smoking has been shown to result in increased levels of
alveolar bone loss with dental implants.
44
Diabetes mellitus has also
been shown to increase the risk for peri-implant disease compared
with healthy individuals.
45
is is due to elevated blood sugar levels
that compromise wound healing and the host immune system.
Management
Peri-implant mucositis is a reversible inammatory process. How-
ever, if not treated properly, the persistent inammatory condition
may progress to peri-implantitis that results in irreversible bone
loss. In most cases peri-implant mucositis is a precursor for the
development of peri-implantitis.
46
Nonsurgical (closed debridement) mechanical debridement
to remove plaque and calculus from the implant surface using
mechanical instruments such as scalers and curettes coupled with
antimicrobial rinse therapies is the primary therapeutic approach
for peri-implant mucositis.
47
In a systematic review, nonsurgical mechanical debridement is
eective in the management of peri-implant mucositis. Use of anti-
septics increased the observed outcomes.
48
It is crucial to implement a
comprehensive patient and professional oral hygiene program to man-
age peri-implant mucositis. Power brushes, interproximal and irriga-
tion power devices, dentifrices, and antimicrobials have been shown
to be highly eective in the management of peri-implant mucositis.
Professional Mechanical Debridement
For the removal of supragingival and subgingival biolm and bacteria,
debridement of the exposed implant surface and implant abutment
must be completed. ere exist many dierent debridement systems.
Curettes. e selection of scalers for titanium implant debride-
ment is important to minimize surface changes after treatment.
Various types of curettes are available for debridement procedures
(Fig. 41.4):
A B
Fig. . Prosthesis-Related Peri-mucositis. (A) Hygiene difficulty because of an (B) When prostheses
are fixed, usually hygiene will be more difficult.
A
B
CD
Fig. . (A) Titanium curette. (B) Carbon-reinforced curette. (C) Teflon/plastic. (D) Steel curette. (A and
B, Courtesy Salvin Dental Specialties, Inc., Charlotte, N.C.)

1147
CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies
• Titanium-coated curettes are specically made for dental
implant debridement because they have a similar hardness to
the titanium surface and will not scratch or mar the surface.
• Carbon-bercurettesaresofterthantheimplantsurfacesand
will not damage the implant surface. ese types of curettes are
prone to fracture.
• Teon curettes are similar to carbon-reinforced curettes and
will not scratch the surface of the implant.
• Plastic curettes have been advocated as the instrument of
choice to prevent damage from the implant surface.
• Stainless-steelcurettesaremuchharderthantitaniumalloyand
are not recommended for use around dental implants because
they may alter the implant surface.
49
Amorphousresinscalerscomewithunlledorlledresin.Unlled
resin scalers have no reinforcements for shape or stiness, whereas
lled resin llers may use materials such as silica, graphite, or glass.
ese scalers have replacement tips on stainless-steel handles.
• Titaniumbrushbursinsertintoimplantmotors.eyhavea
variety of shapes, allowing them to adapt around the implant
or prosthesis surface circumferentially, around a single surface,
and for groove cleaning. Brushes are used at 600 rpm and
adapted against the implant surface to remove debris.
Hasturk etal. evaluated six dierent types of scaler materials
to scratch surfaces of dierent brands of implants abutments,
and they were compared with scanning electron microscopy. e
results showed glass-lled resin curettes caused the most scratches,
whereas the unlled resin scalers had the least surface alteration.
However, these studies are on smooth titanium abutments and
not on the rough implant surface.
50
ere may not be clinical relevance regarding whether curettes
scratch implant surfaces. Anastassiadis etal. reported that metal
scalers do not readily scratch cementum; it is questionable that
a titanium implant surface, which has a higher Mohs hardness,
should be of any concern.
51
Furthermore, scalers as a whole may be eective in removing large
calculus particles or granulation tissues but are rather ineective try-
ing to navigate the perimeter and grooves of an exposed implant
surface. For that reason, curette material may not be a signicant
concern, but rather the activity of curetting may be (Fig. 41.5).
Ultrasonic Devices
Ultrasonic devices with special polyetheretherketone-coated tips
have been used to debride the implant surface. is tip is made of
a plastic material with a stainless-steel core. is ultrasonic device
allows the debridement of plaque and calculus, while leaving a
smooth and clean surface.
Although metal tips are not recommended, plastic tips may be
at an increased risk of shredding when cleaning around implant
A
B
Fig. . Peri-mucositis Treatment. (A,B) Scaling technique around an implant with peri-implant inflam-
mation.

1148
PART VIII Dental Implant Maintenance
grooves and threads. Tips made of PEEK material (Hu-Friedy,
Chicago, Ill.) have been shown to be resistant to shredding and
may be considered (Fig. 41.6).
Antimicrobials
Antiseptics are dened as antimicrobial substances that are non-
damaging to living tissue/skin while reducing the possibility of
infection, sepsis, or putrefaction. Several types of antiseptics are
ready for dental use: chlorhexidine 0.12% or 0.2%, cetylpyri-
dinium chloride, sodium hypochlorite 1.0%, hydrogen peroxide
3.0%, citric acid 40.0%, Ethylenediamine tetraacetic acid (EDTA)
24%, povidone-iodine 10%, and phenols/essential oils.
52,53
For management of peri-mucositis, several qualities are
needed for antiseptics to be eective: biolm penetration, long
substantivity, tissue biocompatibility, and low resistance. Removal
of macrodeposits should be performed with scalers rst.
Chlorhexidine applied on a cotton pellet and burnished
against a machined surface has shown a 92.9% Porphyromonas
gingivalis endotoxin reduction.
54
Povidone-iodine has high anti-
septic capability but has a highly irritating eect if any residue
comes in contact with an osseous structure. Several of the anti-
septics and their eectiveness on Staphylococcus epidermidis, Can-
dida albicans, and S. sanguinis have been investigated. Although
sodium hypochlorite was most eective in the reduction of
all three bacterial biolms, it has the highest tissue toxicity.
Hydrogen peroxide was active against only C. albicans, whereas
chlorhexidine gluconate and phenols/essential oils had activity
against only Streptococcus sanguinis and C. albicans
55
(Fig. 41.7).
Patient At-Home Mechanical Debridement
Implant patients must understand their role in maintaining their
dental implants and implant prosthesis. An individualized home
care assessment and protocol must be developed for each patient,
and it must be customized according to the tissue condition,
implant position, and type of prosthesis. Home care devices that
have been shown to be safe around implant surfaces include tooth-
brushes (manual or powered), oss (e.g., plastic, braided nylon,
coated, stiened ends to clean under pontic areas, and dental
tape). In addition, oral irrigators, interdental brushes, and end-tuft
brushes may be used. (See Chapter 42 for a complete list of home
care aids.) A strong home care regimen may signicantly reduce
the amount and composition of subgingival microbiota around
teeth. is reduction most likely will translate to a decreased risk
for periodontal disease initiation or recurrence. Furthermore, the
decreased prevalence of periodontal pathogens in supragingival
plaque decreases potential reservoirs of these species.
63
Peri-implantitis
e American Academy of Periodontology has dened peri-
implantitis as an “inammatory reaction associated with the
loss of supporting bone beyond initial biologic bone remodeling
Fig. . Ultrasonic scalers may be used to treat peri-mucositis.
A B
Fig. . (A) Chlorhexidine: used as a rinse or locally applied (Peridex; 3M ESPE Dental Products, St.
Paul, Minn.). (B) Local application of chlorhexidine to implant surface.

1149
CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies
around an implant in function.
64
Peri-implantitis has been
shown to exhibit similar microbial ora as chronic periodontitis.
Although there is no consensus regarding microorganisms, Perez-
Chaparro etal.
65
identied three commonly occurring pathogens
associated with peri-implantitis: Porphyromonas gingivalis, Trepo-
nema denticola, and Tannerella forsythia. e dental implant may
exhibit all the signs of peri-implant diseases, including exudate,
increased pocket depths, and crater-like osseous defects, which are
strictly localized around the implant. If left untreated, signicant
bone loss, infection, and mobility could result, leading to loss of
implant osseointegration. Additional clinical signs include radio-
graphic vertical bone loss greater than 2 mm, bleeding on prob-
ing (with or without exudate), mucosal swelling and erythema,
and an absence of pain (Box 41.4). e crestal bone loss may be
induced by stress, bacteria, or a combination of both. A system-
atic review on peri-implantitis
66
identies acknowledged etiolo-
gies and related causes of peri-implantitis.
After bone loss from stress or bacteria occurs, the sulcu-
lar crevice deepens and a decrease in oxygen tension is pres-
ent. Anaerobic pathogenic bacteria may become the primary
promoters of the continued bone loss. An exudate or abscess
indicates exacerbation of the peri-implant disease and possible
accelerated bone loss. Studies have shown the prevalence rate of
peri-implantitis has been found in 28% to 56% of subjects and
12% to 43% of implant sites (Fig. 41.9).
67
Etiology
Peri-implantitis has been associated with a gram-negative anaer-
obic microbiota, similar to that found in severe periodontitis
around natural teeth.
68
Peri-implantitis encompasses similar clini-
cal signs of peri-implant mucositis, but loss of bone and attach-
ment is observed. A stabilized implant that continues to exhibit
loss of bone levels is indicative of peri-implantitis.
Biofilm
Although bacterial biolm insult is identied as the main cause
of peri-implant mucositis, peri-implantitis is considered to be
initiated by stress factors caused by poor biomechanical forces.
In addition, several other etiologic factors exist, such as poor
implant placement, poor oral hygiene, residual cement, host
response, poor implant surface, unfavorable osseous density,
untreated periodontitis, alcohol excess, smoking, untreated end-
odontic lesions, diabetes, among others. Monje etal.,
69
in a sys-
temic review, conrmed that peri-implantitis may be prevented
with a strong peri-implant maintenance program, along with a
comprehensive patient, clinical, and implant-related evaluation.
ey concluded a minimum recall and hygiene program be tai-
lored to the patients risk proling and at a minimum of a 5- to
6-month interval.
Occlusal Stress
Unfavorable stress factors can initiate crestal bone loss, and
bacterial biolm challenges may further enhance the rate
of osseous destruction. In recent studies, bacterial biolms
attached onto the surface of implants were shown to create a
highly acidic environment that causes corrosion, pitting, crack-
ing, etc.
70
Furthermore, recent studies have shed light on the
release of titanium ions from the implant surface, which results
in a signicant increase in a local inammatory response
71
(Table 41.1).
History of Periodontitis
Most long-term studies and systemic reviews have concluded that
patients with a history of periodontitis had a higher incidence of peri-
implantitis in comparison with periodontally healthy patients.
72,73
Papantonopoulos etal.
74
have reported on two implant phenotypes
that are directly related to peri-implantitis. A peri-implantitis-suscep-
tible phenotype was associated with fewer teeth and younger age, and
was predominantly in the mandible. A peri-implantitis-resistant phe-
notype was mainly found in the maxilla.
74
Smoking/Tobacco Use
Although many conicting studies exist on the relationship
between smoking and peri-implantitis, most reports have shown
statistically signicant dierences between smokers and non-
smokers. Rinke etal.
75
reported that smokers had an approxi-
mate odds ratio of 31.58 in development of peri-implantitis. e
overall peri-implantitis rate in their study population was 11.2%
and as high as 53% for patients who smoked and had a history
of periodontitis.
Diabetes
e relationship between diabetes and periodontal disease is well
established. Poorly controlled diabetes has also been associated
with peri-implantitis.
76,77
Venza et al.
78
reported that the long-
term prognosis for dental implants is more favorable when the
patient’s glycosylated hemoglobin (HbA
1c
) is less than 7%.
Canullo etal.
79
proposed an evidence-based classication for
dierent clinical subtypes of peri-implantitis, including: (1) sur-
gically triggered peri-implantitis, (2) prosthetically driven peri-
implantitis, and (3) plaque-induced peri-implantitis. ey state
that these three subtypes of peri-implantitis are separate, dier-
ent entities that may be distinguished with predictive proles.
In addition, various risk factors can act synergistically with a
clinical scenario, which make the causative factors more dicult
(Table 41.2).
79
Prevention
Home Care
An eective oral hygiene program is paramount to minimize peri-
implant disease. is has been shown through various studies.
Direct correlations between poor oral hygiene and peri-implant
bone loss in a 10-year follow-up study were reported.
80
Other stud-
ies have shown a correlation with poor oral hygiene and a higher
plaque score.
81
In addition, patients who have lost their teeth to
periodontal disease are more susceptible to peri-implantitis.
82
Professional Care
orough periodontal charting and review is essential. Patients
with periodontitis must have this pathologic condition controlled
before implant placement. Patients who do not demonstrate the
• Verticalboneloss(radiographic,probing,orboth)
• Peri-Implantpockets
• Bleedingonprobing
• Exudate
• Mucosalswelling
• Erythema
• Usuallynoassociatedpain
BOX
41.4
Clinical Symptoms Associated With
Peri-Implantitis

1150
PART VIII Dental Implant Maintenance
ability to maintain oral hygiene need to be educated and put on
stringent professional care regimens.
Prosthetic Design
A thoroughly evaluated cone beam computed tomography scan
study with favorable biomechanical design for prosthetics is man-
datory. Ideal implant position is paramount to allow for a properly
designed prosthesis that is cleansable.
Cementation Technique
e meticulous use of cements when delivering a prosthe-
sis is imperative, or the clinician can choose to use a screw-
retained prostheses. If a cementable prosthesis is utilized,
the clinician must take precautions to prevent retainment
of cement. Conventional cementable techniques that are
normally used for natural teeth are not recommended (See
Fig. 41.5).
AB
C
D
E
Fig. . Peri-Implantitis. (A and B) Clinical images depicting bone loss. (C) Radiograph showing sig-
nificant bone loss around implant. (D) Cratering bone loss. (E) Implant failure caused by calculus formation.

1151
CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies
Human Studies on Peri-Implantitis Treatment
Author Procedure
Number of Patients
and Implants and
Time of Follow Up Treatment Outcome
Leonhardt
etal2003
Accesssurgery 9patients
26implants
60months
Systemicantibiotics(accordingtomicro-
biologicanalysis)+accesssurgery+
decontaminationoftheimplantsurface
using10%hydrogenperoxide
0.2%CHX2×adayrinse
Healing:58%oftheimplants
7implantslost
4/19ongoingboneloss
6/19bonegain
Meangingivalbleedingwasreducedfrom
100%–5%
Diseaseprogressionat2otherimplants
Romeoetal
2007
Apicallyrepositioned
apsurgery+
implantsurface
modication
Resectivesurgery
19patients
38implants(11hol-
lowscrewand7
solidscrew)
12–24–36months
Systemicantibiotics(amoxicillinfor8days)
+fullmouthdisinfection
9patientswithresectivesurgeryand10
withresectivesurgeryandmodication
ofsurfacetopography
Implantsurfacedecontaminationwith
metronidazolegel,tetracyclinehydro-
chloride,andsaline
Radiographicassessment:
Implantoplastyisaneffectivetreatment
procedure
Signicantlybetterresultsw/apicalreposi-
tionapsurgery+implantsurface
modication
Behnekeetal
1997
Bonegraftsandbone
graftsubstitutes
surgery
• Nonsubmerged
10patients
14implants
6months–2years
Irrigationwithiodine+systemicantibiotics
(Ornidazole500mg×2for7days)
Implantsurfacetreatedwithairpowder
andirrigationwithsaline
7implantswith2–3walldefectsgotbone
chipsand7implantswith1walldefect
gotboneblocks
Clinical:(6months/14implants)
BI:2.4–0.3
PD:5.9–2.3mm
Clinical:(2years/5implants)
BI:2.4–0.4
PD:5.9–2.5mm
Radiographic:(3–12months/14implants)
Averagebonell:3mm
Behnekeetal
2000
Bonegraftsandbone
graftsubstitutes
surgery
• Nonsubmerged
25implants
6monthsto3years
Irrigationwithiodinefor1month+
debridementwithmucoperiostealap
surgery
Implantsurfacedecontaminationwithair
abrasiveinstrumentsfor30seconds+
salineirrigation+7bonechipsand18
boneblocks(Metronidazole400×2
for7days)
Clinical:(1year/18implants)
PD:5.3–2.2mm
Clinical:(3year/10implants)
PD:5.3–1.6mm
Radiographic:(1year/18implants)
Meanbonell:3.9mm
Radiographic:(3year/10implants)
Meanbonell:4.2mm
Aughtunetal
1992
Barriermembranes
• Nonsubmerged
12patients
15implants
6–12months
ePTFEmembrane+systemicantibiotics
(tetracycline200mg×1for12days)
+implantdetoxication(airpowder)+
irrigationwithsaline
Clinical:
PI:1.9–1.0
BI:1.1–1.1
PD:5.2–4.1mm
Radiographic
Meanboneloss:0.8mm
Minorimprovementsonsofttissue
conditions
Membraneexposure
Jovanovic
etal1992
Barriermembranes
• Nonsubmerged
7patients
10implants
6monthsto3years
ePTFEmembrane+systemicantibiotics
(Tetracycline250mg×4for7days)
+implantdetoxication(air-powder+
chloramineT+salineirrigation)
Clinical:
PI:1.7–0.6
GI:2.1–0.3
PD:6.8–4.1mm
Allclinicalsignsimproved
Radiographically:
7defectsshowedbonell
3defects:nobonell
TABLE
41.1
Continued

1152
PART VIII Dental Implant Maintenance
Author Procedure
Number of Patients
and Implants and
Time of Follow Up Treatment Outcome
Khouryand
Buchmann
2001
Graftingmaterials
+barrier
membranes
25patients
41implants
36months
Systemicantibiotics
Group1(12implants):detoxicationwith
chlorhexidineirrigation+citricacid
+hydrogenperoxide+saline+bone
blocksandparticulatebone
Group2(20implants):treatmentsasgroup
1+ePTFE
Group3(9implants):treatmentsasgroup
1+collagenmembrane(submerged)
Clinical:
1:PDreductions:5.1mm
2.PDreductions:5.4mm
3.PDreductions:2.61mm
Radiographic:
2.4mmbonell
2.8mmbonell
1.9mmbonell
58.6%ofthebarriertreatedimplantsites
werecompromisedbyearlypost
therapycomplications
Theadditionalapplicationofbarriersdoes
notimprovetheoveralltreatment
outcomes3yearsfollowingtherapy
Mattoutetal
1995
Withandwithoutgraft-
ingmaterial
19patients 23defects:ePTFEalone
11defects:ePTFE+DFDBA+hydrated
tetracycline
Postoperative:0.1%CHX+amoxicillin500
mg(2×for8days)
Meansuccessrate68%forthemembrane
groupand90%forthemembrane+
boneallograft
Schwarzetal
2006
Graftingmaterials
+barrier
membranes
• Nonsubmerged
22patients
22implants
6months
Granulationtissueremoved+implantsur-
facedebridementwithplasticcurettes
+irrigationwithsaline
Group1:NanocrystallineHA
Group2:Bovinexenograft+resorbable
collagenmembrane
Clinical:
1:PD:reductions:2.1mm
2.PD:reductions:2.6mm
“Inbothgroups,radiologicobservation
revealedadecreasedtranslucency
withintheintrabonycomponentofthe
respectiveperi-implantbonedefect.”
Additionally,bothtreatmentsresultedin
clinicallyreductionsinPDandgainsof
CALat6monthsaftersurgery
Schwarzetal
2008
Graftingmaterials
+barrier
membranes
• Nonsubmerged
22patients
2years
Group1:Accessapsurgery+nanocrys-
tallinehydroxyapatite
Group2:Accessapsurgery+natural
bonemineral+collagenmembrane
2patientsinNHA:severepusformationat
12months
Clinically:
PD:
Group1:1.5±0.6mm
Group2:2.4±0.8mm
CALgains:
Group1:1.0±0.4mm
Group2:2.0±0.8mm
Bothtreatmentsshowedefcacyover2
years.Naturalbonemineral+collagen
membraneshowedbetterclinical
improvements
Roos-
Jansaker
etal2007a
Graftingmaterials
+barrier
membranes
• Nonsubmerged
36patients
65implants
12months
Systemicantibiotic(amoxicillin375×3+
metronidazole400mg×2)for10days
starting1daybeforesurgery
Debridementofthegranulationtissue,
implantsurfacedecontaminationwith
hydrogenperoxideandirrigatedwith
saline
GroupI:Bonesubstitute+resorbable
membrane
Group2:Bonesubstitutebutnomembrane
Group1:
PDreduction:2.9mm
Meanbonell:1.5mm
Group2:
PDreduction:3.4mm
Meanbonell:1.4mm
Human Studies on Peri-implantitis Treatment—cont’d
TABLE
41.1

1153
CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies
Author Procedure
Number of Patients
and Implants and
Time of Follow Up Treatment Outcome
Roos-
Jansaker
etal2007b
Graftingmaterials
+barrier
membranes
Submerged
12patients
16implants
12months
Systemicantibiotics(amoxicillin375×3+
metronidazole400mg×2)for10days
starting1daybeforesurgery.Debride-
mentofgranulationtissue.Implant
surfacedecontaminationwithhydrogen
peroxideandirrigationwithsalineBone
substitute+resorbablemembrane
Clinicalandradiographicimprovements
wereobserved.
PDreduction:4.2mm
Meanbonell:2.3mm
Haasetal
2000
DiodeLaser
treatment
duringsurgery
17patients
24implants
3–9.5months
Implantsurfacedecontaminationwith
curettage+laser+defectlledwith
autogenousbone+ePTFEmembrane+
systemicantibioticsfor5days
Radiographically:
3monthsfromtimeofmembrane
removal:21.8%
9.5months:meanbonegain:36.4%
Bachetal
2000
DiodeLaser
treatment
duringsurgery
30patients
5years
Group1:Scaling+1.5%CHX+openap
debridement,apicalrepositioningthe
ap+osseousaugmentationand/or
mucogingivalcorrections
Group2:Treatmentsasgroup1+laser
decontaminationwithdiodelaser(810
nmw/6W)
Group1:
18months:noincreasedPD,BOPor
signofinammatoryprocess
2years:2patientswithincreasePD,
BOPandclinicalsignofinam-
mation
4years:5patientswithincreasePD,
BOPandclinicalsignofinam-
mation
Between3and5years:
4implantsremoved
Group2:
3years:norelapse
5years:5patientswithincreasePD
andclinicalsignsofinammation
Noimplantremoved
Signicantreductionofgram-negative,
anaerobicbacteriainlasergroup
thanconventionalgroup
Dortbudak
etal2001
Diodelaser
treatment
duringsurgery
15patients
15implants
Implantsurface:Curettage+rinsingwith
salinefor1minute,thenstainedwith
toluidine
Halfoftheimplantsfurthertreatedwith
diodelaserfor1minute
TBOaloneresultsinasignicantbacterial
reductionofP. intermediaandAAon
plasmaame-sprayedcontaminated
implantsurfaces,whileacombined
treatmentleadstoareductiontoAA,
P. gingivalis,andP. intermedia.
Completeeliminationofbacteriawas
notachieved
Romanosand
Nentwig
2008
CO
2
laser+bone
augmentation+
membrane
15patients
27.10±17.83
months
Openapdebridementw/titaniumcurettes
+CO
2
laser(2.84±0.83watts)for1
minute
Boneaugmentation(bovineorautogenous
bone)andcollagenmembrane
Nosystemicantibiotics
PI:
Preoperative:1.01±1.37
Postoperative:0.98±1.20
BI:
Preoperative:2.76±0.35
Postoperative:1.03±0.85
PD:
Preoperative:6.00±2.03mm
Postoperative:2.48±0.63mm
Keratinizedtissue
BI:
Preop:2.30±1.45mm
Postop:2.41±1.39mm
Human Studies on Peri-implantitis Treatment—cont’d
TABLE
41.1
Continued

1154
PART VIII Dental Implant Maintenance
Author Procedure
Number of Patients
and Implants and
Time of Follow Up Treatment Outcome
Deppeetal
2007
CO
2
laser+bone
augmentation
32patients
73implants
4monthsand5years
Group1(19implants):Softtissueresection
+conventionaldecontamination
Group2(15implants):Treatmentasgroup
1+βTCP+autogenousbonegrafts
Group3(22implants):Softtissueresection
+CO
2
laserdecontamination
Group4(17implants):Treatmentasgroup
3+βTCP+autogenousbone
3implantslostingroup1
4implantslostingroup2
2implantslostingroup3
4implantslostingroup4
Beginningofhygienephase
PI:
Group1:1.8±1.2
Group2:1.4±1.2
Group3:1.4±0.9
Group4:2.6±0.5
BI:
Group1:2.7±0.9
Group2:2.3±1.4
Group3:2.8±1.2
Group4:3.3±0.6
PD:
Group1:6.2±1.8
Group2:5.1±1.7
Group3:5.7±1.4
Group4:5.7±1.4
Immediatelybeforesurgery
PI:
Group1:0.7±0.8
Group2:0.9±0.4
Group3:0.7±0.8
Group4:0.5±0.6
BI:
Group1:0.7±0.8
Group2:0.5±0.8
Group3:0.6±0.3
Group4:1.2±0.6
PD:
Group1:5.1±1.3
Group2:4.8±1.4
Group3:6.1±1.6
Group4:5.0±1.3
4months
PI:
Group1:0.6±0.7
Group2:0.6±0.6
Group3:0.8±0.6
Group4:0.5±0.4
BI:
Group1:0.9±0.5
Group2:0.6±0.6
Group3:0.7±0.6
Group4:0.9±0.8
PD:
Group1:3.2±0.9
Group2:2.4±0.7
Group3:2.1±1.3
Group4:1.0±0.7
5years
Human Studies on Peri-implantitis Treatment—cont’d
TABLE
41.1

1155
CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies
Author Procedure
Number of Patients
and Implants and
Time of Follow Up Treatment Outcome
PI:
Group1:0.8±0.8
Group2:1.1±0.8
Group3:1.0±1.3
Group4:1.2±1.3
BI:
Group1:1.1±1.2
Group2:2.1±1.4
Group3:1.8±1.1
Group4:1.9±1.0
PD:
Group1:4.3±1.2
Group2:2.5±1.1
Group3:3.4±1.5
Group4:2.5±1.4
Treatmentofperi-implantitismaybeac-
celeratedbyusingaCO
2
laser+soft
tissueresection
Long-termresultsinaugmenteddefects,
nodifferencebetweenlaserand
conventionaldecontamination
Froumetal
2012
Regenerativeapproach
Biologics+bone+
membrane
51implants
38patients
3–7.5years
Systemicantibiotics(2000mgamoxicillin
or600mgclindamycin)1hrbefore
surgeryandcontinue500mgamoxicil-
lintidorclindamycin150mgqidfor
additional10days
Surfacedecontaminationw/bicarbonate
powderfor60seconds(airabrasive
device),60-secondirrigationwithster-
ilesaline,tetracycline(50mg/mLwith
cottonpelletsorbrushfor30seconds,
thensecondbicarbonateairabrasion
60seconds,applicationof0.12%
CHXfor30seconds,then60seconds
reirrigationwithsterilesaline+enamel
matrixderivatives+anorganicbovine
bonesoakedinplateletderivedgrowth
factorforatleast5minutesormin-
eralizedfreeze-driedbone+collagen
membraneorsubepithelialCTgraftat
area(<2mmKG)
Group1:Greatestdefectdepthradiographi-
cally
Group2:Greatestbonelossonthefacial
ofimplant
•Noimplantlost
•PDreduction:
Group1:5.4mm
Group2:5.1mm
•Bonelevelgain:
Group1:3.75mm
Group2:3mm
AA, Aggregatibacter actinomycetemcomitans; BI, Bleeding index; BOP, Bleeding on probing; BTCP, Beta Tricalcium Phosphate; CAL, Clinical attachment level; CHX, Chlorhexidine; DFDBA, Demineralized
freeze-dried bone allograft; ePTFE, expanded polytetrafluoroethylene; GI, Gingival Index; HA, Hydroxyapatite; KG, Keratinized gingiva; NHA, Nanocrystalline Hydroxyapatite; PD, Probing depth; PI, Plaque
index; TBO, toluidine-blue-O.
From Suzuki JB, Misch CE. Periodontal and maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implantology. St. Louis, MO: Elsevier; 2018.
Human Studies on Peri-implantitis Treatment—cont’d
TABLE
41.1
Control of Parafunctional Forces
An occlusal guard is crucial in preventing unfavorable occlusal
stress. e night guard is adjusted to be on a at plane occlusion
to disperse stress. Careful discussion should be conducted with
the dental laboratory to convey the desired design for successful
clinical outcomes.
Management
e objective of treatment for peri-implantitis is for osseous regen-
eration of the implant-bone defect. However, such treatment has
been challenging because the implant surface needs to be detoxi-
ed, along with modifying the soft and hard tissues. is may
involve nonsurgical and surgical treatment.

1156
PART VIII Dental Implant Maintenance
Nonsurgical Management of Peri-Implantitis
Nonsurgical treatment of peri-implant mucositis is often success-
ful. In contrast, the nonsurgical treatment for peri-implantitis
is not as predictable. is is most likely due to the inability to
remove the bacterial biolm from the exposed implant surface.
Such diculty has been especially observed with rough surface
dental implants.
83
A systematic review illustrated that implant
surfaces and diameter are potential risk factors for bone loss and
peri-implantitis.
84
e nonsurgical treatment of peri-implantitis usually involves
the debridement and detoxication of implant surfaces, similar to
the treatment of peri-implant mucositis. However, the issue that
arises is that these exposed surfaces usually have concurrent sub-
gingival pockets.
Low-Abrasive Amino Acid Glycine Powder. Low-abrasive
amino acid glycine powder has been shown to be an eective treat-
ment for removing biolm without damaging the implant surface,
and hard and soft tissues of the periodontium. is technique uses
a special handpiece with a plastic tube nozzle with three orthogo-
nally oriented holes. An air-powder mixture with reduced pressure
is expelled through the nozzle, which prevents the formation of air
emphysema complications. e nozzle is moved in a circumferen-
tial movement around the implant surface.
85
Although more extensive studies need to be conducted as to
technique ecacy, glycine powder can be incorporated into a
treatment regimen. e clinician should be careful to use the pow-
der only in areas where access is available, including a posttreat-
ment rinse to remove any residue. is modality is best used in
cases with a buccal dehiscence and/or horizontal bone loss with-
out crater or infrabony pocketing. An air-powder unit (Hu-Friedy,
Chicago, Ill.) that adapts to a slow-speed handpiece is available
and may be used eectively (Fig. 41.10).
Ultrasonic Devices. For treatment of peri-implantitis, tip
modications (i.e., carbon ber, silicone, or plastic) must be used.
Care must be exercised not to use metal tips as they may alter
the implant surface. Ultrasonic devices should be used only when
plastic tips are available. Irrigation and meticulous cleaning are
recommended in treatment for either open ap debridement or
closed ap irrigation.
Lasers. One of the newer and least invasive methodologies to
treat peri-implant mucositis and peri-implantitis involves the use
of laser photonic energy, a coherent form of infrared or visible
light, usually of a single wavelength. Lasers have been used eec-
tively for decades in oral implantology in second-stage recovery
of implants through the ablation and vaporization of overlying
soft tissue.
86
Laser Protocols. Similar to their use in treating periodontal
disease, lasers provide dierent treatment approaches for peri-
implantitis: nonsurgical, surgical, antimicrobial photodynamic
therapy, and photobiomodulation.
• Nonsurgical: In the nonsurgical modality, lasers are used
adjunctively to help remove calculus, reduce inammation and
remove diseased soft tissue, and reduce subgingival pathogens.
Using dierent types of lasers, such as the diode, Nd:YAG
(neodymium-doped yttrium aluminum garnet), erbium, or
carbon dioxide laser, the laser beam is directed at the inamed
soft tissue within the sulcus, using noncontact overlapping
strokes to disrupt the biolm, reduce the microbial popula-
tion, and decontaminate the pocket epithelium. Erbium lasers
have also been shown to remove calculus from the implant
surface.
87-95
• Surgical: Minimally invasive laser-assisted surgical techniques
involve removal of diseased epithelial lining. More invasive
surgical procedures involve conventional elevation of a full-
thickness ap for surgical access, followed by laser-assisted
degranulation, surface debridement and decontamination,
and osseous tissue removal or recontouring. As indicated, bone
augmentation may be performed through placement of bone-
grafting material.
96-103
• Antimicrobial Photodynamic erapy: Antimicrobial photody-
namic therapy in periodontology is a light-based approach to ter-
minating bacteria. A photoactivatable substance (photosensitizer)
is applied to the targeted area (i.e., within the sulcus) and then
activated by laser light. Singlet oxygen and other cytotoxic reac-
tive agents are produced to reduce periodontopathogens.
104-109
• Photobiomodulation: is a form of light therapy that uses non-
ionizing forms of light, including lasers in the visible and
infrared spectrum. e nonthermal technique is used to elicit
photophysical and photochemical events. In implantology, it is
used to promote wound healing and tissue regeneration. It has
also been shown to increase osteoblastic proliferation, collagen
deposition, and bone neoformation.
110-115
Although laser-based peri-implantitis treatment techniques
are generally positive, some studies indicate adjunctive use
of lasers have limited or no extra benecial eect compared
with conventional treatment methodologies. Additional well-
designed, long-term, randomized controlled trials are needed
to verify the clinical and microbiologic outcomes of laser
use.
116-118
Assurance of positive therapeutic outcomes is facilitated by an
informed clinical technique, prudent use of proper laser operating
parameters, and awareness of all laser wavelengths. However, when
used inappropriately, laser energy can adversely alter implant sur-
faces and/or induce undesirable temperature increases, which may
be detrimental to implant health
119-122
(Fig. 41.11).
In 2014 a human clinical study consisting of 16 patients was
published, using a pulsed 1064-nm Nd:YAG laser (PerioLase
MVP-7; Millennium Dental Technologies, Cerritos, Calif.). e
technique introduced is known as the Laser-Assisted Peri-Implan-
titis Protocol (LAPIP) to manage patients with peri-implantitis
123
without the use of bone augmentation (Fig. 41.12). (LAPIP is
Predictive Proles Associated With
Peri-Implantitis
223,224
Risk Factor Predictive Profiles
Type 1:surgicalfactors • Presenceofplaqueassociatedwith
orovestibularandmesiodistalimplant
malpositioning
• Failedbonereconstruction
Type 2:prosthetic
factors
• Plaqueassociatedwithretainedcement
remnants
• Nonidealnishlinemargin(2mm
belowsofttissuemargin)
• Occlusaloverloading
• Prosthesismaterialfracture
• Abutmentscrewloosening
• Implantfracture
Type 3:plaque-induced Generalizedbone-levelrecessionassociated
withplaqueaccumulation,withoutany
surgical/prostheticcomplication
TABLE
41.2

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114241Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesJON B. SUZUKI AND KEVIN R. SUZUKIImplant dentistry has evolved into an evidence-based, clinical science with well-documented research to validate previously unsupported clinical practice procedures. Sig-nificant efforts that focus on the biology and biomechanics of implant dentistry have helped to develop and refine clinical techniques based on peer-reviewed findings. However, despite improved and predictable clinical successes in implantol-ogy, peri-implant diseases have been diagnosed with increas-ing incidence. The evolution of research and understanding of biologic concepts in implant dentistry and implant rescue has caused many areas of debate and controversy. Innovative theories have been developed that have resulted in technique modifications. Science has spurred implant dentistry to new pinnacles of success, which is highly based upon essential principles of periodontal regeneration.e tremendous expansion of knowledge in implant dentistry has created new ideas and terminology that is redened based on new applications to implant dentistry. In many instances new research may contradict established paradigms. It may be chal-lenging for clinicians to select correct protocols, procedures, armamentarium, and techniques. As materials and techniques are further investigated, dogma may undergo criticism and con-troversy. Experienced clinicians consistently introduce and rene techniques and instruments to maintain clinical excellence as technology and research advance.One area of expansion of knowledge and views relates to the maintenance of dental implants. Early research explored techniques and instruments that were current for the methods and materials of that era. Although many of those implants are still in function in patients today, research and advances in technology have given us newer materials, implant design, and protocols to maintain dental implant health.An understanding of the mucoepithelial implant attachment is essential before commencing maintenance procedures. Contro-versies and parameters for probing and crestal bone loss are impor-tant for clinicians to recognize. ere are anatomic and histologic dierences between the attachment apparatus of teeth compared with implants that are osseointegrated. e bacterial plaque bio-lm on these implant-tissue attachments may be signicant to clinical success.When the clinician understands the parameters of implants and teeth, specic maintenance plans may be established for the patient to minimize the possibility of developing peri-implant dis-ease. Clinicians should inform patients of expectations and out-comes during treatment, and demonstrate oral hygiene options appropriate during each stage. Patients need to recognize the importance of maintenance protocols, and clinicians should assess compliance to home care routines. Patients also should be com-petent to perform home maintenance. ese strategies would cer-tainly minimize risks for peri-implant disease and implant failures.As the acceptance of and demand for dental implants increase, the need to understand the importance of maintenance as it relates to long-term implant success also increases. e role of the dental hygienist in implant maintenance and care as well as diagnosing peri-implant disease is increasing and becoming more dened.Implants and associated prostheses are much dierent from nat-ural teeth and may require adjunctive procedures and instruments for professional and patient care. Complications may arise when clinicians fail to comprehend these dierences, because they may adversely impact the implant’s outcome, increasing the morbidity of treatment. e techniques and protocols used must be eective at removing biolms and accretions, and procedures performed by patients and clinicians should avoid damage to the components of the implant, abutment, restoration, and associated tissue.Establishment and maintenance of the soft tissue seal around the transmucosal portion of the implant enhances the success of an implant. is barrier is fundamentally a result of appropriate wound healing and connection of epithelial attachments. e maintenance of healthy peri-implant tissues contributes to implant success and minimizes peri-implant disease. In addition, tissues free of inammation and a biolm-controlled implant sulcus will support the patient’s general and oral health. 1143CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesPeri-implant DiseaseOne important, but often neglected, component of comprehen-sive dental implant treatment is the postprosthetic evaluation and treatment of peri-implant issues. ere are many conicting opin-ions and controversies on the diagnosis and treatment of these complications. Failure to eectively and promptly diagnose and treat peri-implant disease with dental implants leads to an increase in implant and prosthetic failure.Dental professionals are initially trained to have a rm under-standing of the disease processes associated with the natural denti-tion. A variety of tests, indices, and radiographic signs are used to determine the health of a natural tooth. Dental implants and their related prostheses have fundamentally dierent relationships to the oral environment than teeth, and these dierences necessitate a change in diagnostic protocol for the determination of health. Failure to understand these processes may lead to undiagnosed disease states and potential morbidity of the implant system.e implant clinician must have a strong understanding of the anatomic and histologic dierences between natural dentition and the dental implant as they pertain to periodontal structures. By having this foundation, the clinician may appreciate these neces-sary dierences and will be better equipped to eectively diagnose peri-implant disease processes. With the increase in the number of dental implants being placed each year, a resultant increase in the incidence of peri-implant disease has been seen. Two condi-tions of peri-implant disease are peri-implant mucositis and peri-implantitis.1 e 6th European Workshop on Periodontology in 2008 concluded that peri-implant diseases are infectious in nature and are dened by “changes in the level of crestal bone, presence of bleeding on probing, and/or suppuration; with or without deep-ening of the peri-implant pockets.”2In dierentiation between these two peri-implant conditions, both have been shown to be localized around implants and dem-onstrate features similar to adult chronic periodontal disease.3 ese conditions may be analogous to gingivitis (peri-mucositis) and periodontitis (peri-implantitis). However, biologic dierences exist between the natural teeth and implants. Basically, peri-implant tissues are more susceptible to infections, due to dier-ences in soft tissue attachment and biolms that may advance to the alveolar-implant complex (see discussion in Chapter 42).4Gingivitis is a bacteria-induced inammation involving the region of the marginal gingiva above the crest of bone and adjacent to a natural tooth. e most common forms are associated with plaque and may be classied as: (1) acute necrotizing, (2) ulcerative, (3) hormonal, (4) drug induced, or (5) spontaneously occurring.5 ese categories may also relate to the gingival tissues around an implant.6,7 e classication of gingivitis and periodontitis has cur-rently been updated by the American Academy of Periodontology.8e bacteria responsible for gingivitis around a tooth may aect the epithelial attachment, without loss of connective tissue attachment. Because the connective tissue attachment of a tooth extends an average of 1.07 mm above the crestal bone, at least 1 mm of protective barrier above the bone is present. In contrast, no connective tissue attachment zone exists around an implant because there is an absence of connective bers that extend into the implant surface. erefore no connective tissue barrier exists to protect the crestal bone around an implant.9Periodontitis around teeth is characterized by apical movement of junctional epithelium and periodontal attachment, coupled with loss of alveolar bone. Bacteria are thought to be responsible by stimulating the body’s immune response, which results in an overall resorptive eect on the periodontal attachment appara-tus. e American Academy of Periodontology (2018) recognizes stages of periodontitis: stage 1, stage 2, stage 3, and stage 4. For-mer specic subtypes10 for each category such as adult chronic periodontitis, rapidly progressive periodontitis, localized juvenile, and prepubertal periodontitis are now encompassed within stage 1, stage 2, and stage 3 of periodontitis.In contrast with teeth, early crestal bone loss around an implant body prosthetically may not always be caused by pathogens. In many cases, the associated bone loss may result from stress fac-tors too great for the immature, incompletely mineralized bone-implant interface or an extension of the biologic width onto a smooth metal crest module.11 erefore, an implant may exhibit early crestal bone loss with a dierent mechanism or cause, com-pared with natural teeth. However, bacteria in some cases may be the primary factor, because anaerobic bacteria have been observed in the microgap between the implant and the abutment or in the sulcus of implants. is is especially evident when sulcus depths are greater than 5 mm (Box 41.1).12 A systematic review13 high-lights potential etiologies of early crestal bone loss around recently osteointegrated implants.In summary, periodontal disease that develops around dental implants has been classied into two separate entities: peri-implant mucositis and peri-implantitis. Peri-implant mucositis is dened as a reversible inammatory reaction in the peri-implant tissues surround-ing an implant. Peri-implantitis is dened as an inammatory reac-tion, with loss of supporting bone around an implant (Fig. 41.1).The Role of Biofilm in Peri-Implant Diseasee oral biolm originates from bacteria and saliva, which result in sticky masses of bacteria with a polysaccharide matrix that accu-mulate on hard and soft surfaces in the oral cavity. e bacterial and biolm formation may adhere to any implant surfaces in the oral cavity and have been reported to result in pocket formation and loss of the supporting bone.14-16 Di Giulio etal.17 determined that biolm is one of the major causes of implant failure. e Consensus of the 7th European Workshop on Periodontology stated that peri-implant infections are always caused by plaque and its by-products (i.e., biolm).18e role of biolms has been heavily studied and has been reported to be responsible for approximately 65% of peri-implant diseases.19 After exposure of the implant surface to the oral cav-ity, a pellicle is formed in less than 30 minutes.20 e pellicle is derived from the saliva, various bacteria present in the oral cavity, and also host tissue products. After formation of the pellicle, bac-terial attachment occurs by cell-to-cell adhesion on the implant surface.21 Most bacteria use biolm as the primary method of Shallow• Gram-positivefacultativecocci,rods• Gram-negativeanaerobiccocci,rods• Motilerods• Spirochetes• Black-pigmentedbacteroides• FusobacteriumDeep• Vibriosorganisms • BOX 41.1 Common Bacteria Associated With Pocket Depths 1144PART VIII Dental Implant Maintenancegrowth, because they facilitate nutrient exchange and prevent competing microorganisms.22 Studies have shown the process of biolm colonization is the same on teeth as with dental implants.23erefore the most ideal solution to prevent microbial infec-tions is to decrease the colonization of bacteria on implant sur-faces. Unfortunately, many characteristics (e.g., material, surface roughness) of prosthetic and implant surfaces directly aect the bacterial adhesion and biolm formation.24For reversal of the peri-implant disease process, the biolm must be removed with mechanical debridement or chemical oblit-eration. If not removed, mature plaque will form. It has been shown that bacteria will migrate from teeth to implants and from implant to implant. Similar to teeth, clinical ndings of failing implants include inammation, pocket formation, and progres-sive bone loss.25e microorganisms may initiate an inammatory release of cytokines that will enhance accumulation of neutrophils to the implant lesion. is process will continue to attract more leuko-cytes and continue to facilitate more peri-implant tissue damage and inammation.26,27 If the inammation progresses, it will lead to peri-implantitis, with the characteristic feature of bone loss around the implant. If left untreated, stromal tissue cells may also propagate, leading to an increase in inltrates of proinam-matory cells that promotes further tissue breakdown,28-30 which may eventually lead to loss of osseointegration, implant mobility, and ultimately implant failure.31-33 In addition to the results of a systematic review, there is evidence that the pathogens Prevotella intermedia, Campylobacter rectus, Aggregatibacter actinomycetem-comitans, and Treponema denticola have been implicated in the pathogenesis of peri-implantitis.34,35Current chemotherapeutics cannot penetrate thick biolm, because rough surfaces have been found to hold more biolm than smooth surfaces.36 Bacterial deposits produce exotoxins and lipopolysaccharides (endotoxins) that inhibit broblast and osteo-blastic growth, and thus prevent proximal regeneration onto the implant surface. Although it is impossible to guarantee 100% ste-rility of exposed implant surfaces, the body is capable of removing small amounts of bacterial deposit via host defense mechanisms.37Carefully removing macrodeposits of plaque biolm and irri-gating with antimicrobial solution is generally sucient to allow a favorable environment for new attachment formation. It is rec-ommended that patients complete a full-mouth debridement to reduce bacterial colonies, including plaque biolms on exposed implant surfaces (Box 41.2). Peri-implant MucositisPeri-implant mucositis is an inammatory condition of the soft tis-sue surrounding an implant, which is similar to gingivitis around natural teeth. In both animal and human studies, peri-implant mucositis has been shown clinically and histologically to be com-parable to gingivitis around natural teeth.184 is has been dened A BC D• Fig. . (A) Spongiotic gingivitis exhibiting erythematous marginal tissue with cyanotic tissue. (B) Peri-odontitis: mandibular anterior exhibiting severe horizontal bone loss. (C) Peri-mucositis: erythematous buc-cal gingiva with associated bleeding around implant crown. (D) Peri-implantitis: significant bone loss with erythematous tissue with significant plaque accumulation. (From Suzuki JB, Misch CE. Periodontal and maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implan-tology. St. Louis, MO: Elsevier; 2018.) 1145CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesBacteriaPrevotella intermediaPorphyromonas gingivalisAggregatibacter actinomycetemcomitansTannerella forsythia (formerly Bacteroides forsythus)Treponema denticolaPrevotella nigrescensFusobacterium nucleatumEtiology• PoorOralHygiene• PoorCompliancewithSupportiveProcedures• PoorProsthesisDesign• PoorFitofProsthesis• Non-idealImplantPosition• LackofNon-KeratinizedPeri-ImplantMucosa• RetainedCement • BOX 41.2 Bacteria and Etiology of Peri-Implant MucositisABC• Fig. . Peri-mucositis. (A) Bleeding on probing without bone loss with a diagnosis of peri-mucositis. (B) Inflammation on the buccal aspect of the mandibular first molar implant. (C) Maxillary overdenture causing peri-mucositis and fungal infections.implant level.39 Clinically, bleeding on peri-implant probing with mucositis may be present without suppuration. If peri-mucositis is allowed to progress, peri-implantitis may result, which includes loss of bone and possible loss of osseointegration, similar to loss of attachment and bone with periodontitis. e relationship between plaque accumulation and peri-implant mucosal inammation has been proven through numerous studies (Fig. 41.2).40-42EtiologyMost cases of peri-implant mucositis are due to poor oral hygiene, inability to clean the implant or prosthesis, nonideal implant position, poor t of the prosthesis, and retained cement. Poorly placed implants or overcontoured prostheses may lead to diculty or inability to properly clean the implants (Fig. 41.3). In addition, peri-implant mucositis may also be caused by titanium alloy hyper-sensitivity. Most dental implants today are covered by a titanium dioxide layer that gives the implant a high surface energy that facilitates the interaction between the host tissues and the dental implant. When the implant becomes exposed to the oral environ-ment, a lower surface energy may provoke a type IV hypersensitiv-ity reaction that may contribute to peri-implant mucositis.43 PreventionBecause of the high prevalence of peri-implant mucositis, it is imperative that the clinician be able to assess the risk prole of each patient and integrate these considerations when treatment as a reversible condition with no loss of attachment or bone loss. e prevalence rate of peri-implant mucositis (bleeding on prob-ing and no loss of bone) in systemic reviews has been shown to be approximately 30% of implants and 47 % of patients.38 How-ever, other studies have reported the incidence to be as high as 80% of patients and 50 % of implants observed. Ferreira etal. reported a prevalence of 64.6% at the patient level and 62.6% at 1146PART VIII Dental Implant Maintenanceplanning is initiated. A consensus report by the Academy of Peri-odontology has shown risk factors to include poor oral hygiene, history of periodontal disease, smoking, retained cement, and occlusal disharmonies. erefore, a comprehensive medical his-tory should be evaluated for any risk factors and the patient should be informed of possible associated complications.Tobacco smoking leads to the end product of nicotine and nor-nicotine that increases cytokine levels and reactive oxygen species. Increased smoking has been shown to result in increased levels of alveolar bone loss with dental implants.44 Diabetes mellitus has also been shown to increase the risk for peri-implant disease compared with healthy individuals.45 is is due to elevated blood sugar levels that compromise wound healing and the host immune system. ManagementPeri-implant mucositis is a reversible inammatory process. How-ever, if not treated properly, the persistent inammatory condition may progress to peri-implantitis that results in irreversible bone loss. In most cases peri-implant mucositis is a precursor for the development of peri-implantitis.46Nonsurgical (closed debridement) mechanical debridement to remove plaque and calculus from the implant surface using mechanical instruments such as scalers and curettes coupled with antimicrobial rinse therapies is the primary therapeutic approach for peri-implant mucositis.47In a systematic review, nonsurgical mechanical debridement is eective in the management of peri-implant mucositis. Use of anti-septics increased the observed outcomes.48 It is crucial to implement a comprehensive patient and professional oral hygiene program to man-age peri-implant mucositis. Power brushes, interproximal and irriga-tion power devices, dentifrices, and antimicrobials have been shown to be highly eective in the management of peri-implant mucositis.Professional Mechanical DebridementFor the removal of supragingival and subgingival biolm and bacteria, debridement of the exposed implant surface and implant abutment must be completed. ere exist many dierent debridement systems.Curettes. e selection of scalers for titanium implant debride-ment is important to minimize surface changes after treatment. Various types of curettes are available for debridement procedures (Fig. 41.4):A B• Fig. . Prosthesis-Related Peri-mucositis. (A) Hygiene difficulty because of an (B) When prostheses are fixed, usually hygiene will be more difficult.ABCD• Fig. . (A) Titanium curette. (B) Carbon-reinforced curette. (C) Teflon/plastic. (D) Steel curette. (A and B, Courtesy Salvin Dental Specialties, Inc., Charlotte, N.C.) 1147CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies• Titanium-coated curettes are specically made for dentalimplant debridement because they have a similar hardness to the titanium surface and will not scratch or mar the surface.• Carbon-bercurettesaresofterthantheimplantsurfacesandwill not damage the implant surface. ese types of curettes are prone to fracture.• Teon curettes are similar to carbon-reinforced curettes andwill not scratch the surface of the implant.• Plastic curettes have been advocated as the instrument ofchoice to prevent damage from the implant surface.• Stainless-steelcurettesaremuchharderthantitaniumalloyandare not recommended for use around dental implants because they may alter the implant surface.49• Amorphousresinscalerscomewithunlledorlledresin.Unlledresin scalers have no reinforcements for shape or stiness, whereas lled resin llers may use materials such as silica, graphite, or glass. ese scalers have replacement tips on stainless-steel handles.• Titaniumbrushbursinsertintoimplantmotors.eyhaveavariety of shapes, allowing them to adapt around the implant or prosthesis surface circumferentially, around a single surface, and for groove cleaning. Brushes are used at 600 rpm and adapted against the implant surface to remove debris.Hasturk etal. evaluated six dierent types of scaler materials to scratch surfaces of dierent brands of implants abutments, and they were compared with scanning electron microscopy. e results showed glass-lled resin curettes caused the most scratches, whereas the unlled resin scalers had the least surface alteration. However, these studies are on smooth titanium abutments and not on the rough implant surface.50ere may not be clinical relevance regarding whether curettes scratch implant surfaces. Anastassiadis etal. reported that metal scalers do not readily scratch cementum; it is questionable that a titanium implant surface, which has a higher Mohs hardness, should be of any concern.51Furthermore, scalers as a whole may be eective in removing large calculus particles or granulation tissues but are rather ineective try-ing to navigate the perimeter and grooves of an exposed implant surface. For that reason, curette material may not be a signicant concern, but rather the activity of curetting may be (Fig. 41.5). Ultrasonic DevicesUltrasonic devices with special polyetheretherketone-coated tips have been used to debride the implant surface. is tip is made of a plastic material with a stainless-steel core. is ultrasonic device allows the debridement of plaque and calculus, while leaving a smooth and clean surface.Although metal tips are not recommended, plastic tips may be at an increased risk of shredding when cleaning around implant AB• Fig. . Peri-mucositis Treatment. (A,B) Scaling technique around an implant with peri-implant inflam-mation. 1148PART VIII Dental Implant Maintenancegrooves and threads. Tips made of PEEK material (Hu-Friedy, Chicago, Ill.) have been shown to be resistant to shredding and may be considered (Fig. 41.6). AntimicrobialsAntiseptics are dened as antimicrobial substances that are non-damaging to living tissue/skin while reducing the possibility of infection, sepsis, or putrefaction. Several types of antiseptics are ready for dental use: chlorhexidine 0.12% or 0.2%, cetylpyri-dinium chloride, sodium hypochlorite 1.0%, hydrogen peroxide 3.0%, citric acid 40.0%, Ethylenediamine tetraacetic acid (EDTA) 24%, povidone-iodine 10%, and phenols/essential oils.52,53For management of peri-mucositis, several qualities are needed for antiseptics to be eective: biolm penetration, long substantivity, tissue biocompatibility, and low resistance. Removal of macrodeposits should be performed with scalers rst.Chlorhexidine applied on a cotton pellet and burnished against a machined surface has shown a 92.9% Porphyromonas gingivalis endotoxin reduction.54 Povidone-iodine has high anti-septic capability but has a highly irritating eect if any residue comes in contact with an osseous structure. Several of the anti-septics and their eectiveness on Staphylococcus epidermidis, Can-dida albicans, and S. sanguinis have been investigated. Although sodium hypochlorite was most eective in the reduction of all three bacterial biolms, it has the highest tissue toxicity. Hydrogen peroxide was active against only C. albicans, whereas chlorhexidine gluconate and phenols/essential oils had activity against only Streptococcus sanguinis and C. albicans55 (Fig. 41.7). Patient At-Home Mechanical DebridementImplant patients must understand their role in maintaining their dental implants and implant prosthesis. An individualized home care assessment and protocol must be developed for each patient, and it must be customized according to the tissue condition, implant position, and type of prosthesis. Home care devices that have been shown to be safe around implant surfaces include tooth-brushes (manual or powered), oss (e.g., plastic, braided nylon, coated, stiened ends to clean under pontic areas, and dental tape). In addition, oral irrigators, interdental brushes, and end-tuft brushes may be used. (See Chapter 42 for a complete list of home care aids.) A strong home care regimen may signicantly reduce the amount and composition of subgingival microbiota around teeth. is reduction most likely will translate to a decreased risk for periodontal disease initiation or recurrence. Furthermore, the decreased prevalence of periodontal pathogens in supragingival plaque decreases potential reservoirs of these species.63 Peri-implantitise American Academy of Periodontology has dened peri-implantitis as an “inammatory reaction associated with the loss of supporting bone beyond initial biologic bone remodeling • Fig. . Ultrasonic scalers may be used to treat peri-mucositis.A B• Fig. . (A) Chlorhexidine: used as a rinse or locally applied (Peridex; 3M ESPE Dental Products, St. Paul, Minn.). (B) Local application of chlorhexidine to implant surface. 1149CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapiesaround an implant in function.”64 Peri-implantitis has been shown to exhibit similar microbial ora as chronic periodontitis. Although there is no consensus regarding microorganisms, Perez-Chaparro etal.65 identied three commonly occurring pathogens associated with peri-implantitis: Porphyromonas gingivalis, Trepo-nema denticola, and Tannerella forsythia. e dental implant may exhibit all the signs of peri-implant diseases, including exudate, increased pocket depths, and crater-like osseous defects, which are strictly localized around the implant. If left untreated, signicant bone loss, infection, and mobility could result, leading to loss of implant osseointegration. Additional clinical signs include radio-graphic vertical bone loss greater than 2 mm, bleeding on prob-ing (with or without exudate), mucosal swelling and erythema, and an absence of pain (Box 41.4). e crestal bone loss may be induced by stress, bacteria, or a combination of both. A system-atic review on peri-implantitis66 identies acknowledged etiolo-gies and related causes of peri-implantitis.After bone loss from stress or bacteria occurs, the sulcu-lar crevice deepens and a decrease in oxygen tension is pres-ent. Anaerobic pathogenic bacteria may become the primary promoters of the continued bone loss. An exudate or abscess indicates exacerbation of the peri-implant disease and possible accelerated bone loss. Studies have shown the prevalence rate of peri-implantitis has been found in 28% to 56% of subjects and 12% to 43% of implant sites (Fig. 41.9).67EtiologyPeri-implantitis has been associated with a gram-negative anaer-obic microbiota, similar to that found in severe periodontitis around natural teeth.68 Peri-implantitis encompasses similar clini-cal signs of peri-implant mucositis, but loss of bone and attach-ment is observed. A stabilized implant that continues to exhibit loss of bone levels is indicative of peri-implantitis.BiofilmAlthough bacterial biolm insult is identied as the main cause of peri-implant mucositis, peri-implantitis is considered to be initiated by stress factors caused by poor biomechanical forces. In addition, several other etiologic factors exist, such as poor implant placement, poor oral hygiene, residual cement, host response, poor implant surface, unfavorable osseous density, untreated periodontitis, alcohol excess, smoking, untreated end-odontic lesions, diabetes, among others. Monje etal.,69 in a sys-temic review, conrmed that peri-implantitis may be prevented with a strong peri-implant maintenance program, along with a comprehensive patient, clinical, and implant-related evaluation. ey concluded a minimum recall and hygiene program be tai-lored to the patient’s risk proling and at a minimum of a 5- to 6-month interval. Occlusal StressUnfavorable stress factors can initiate crestal bone loss, and bacterial biolm challenges may further enhance the rate of osseous destruction. In recent studies, bacterial biolms attached onto the surface of implants were shown to create a highly acidic environment that causes corrosion, pitting, crack-ing, etc.70 Furthermore, recent studies have shed light on the release of titanium ions from the implant surface, which results in a signicant increase in a local inammatory response71 (Table 41.1). History of PeriodontitisMost long-term studies and systemic reviews have concluded that patients with a history of periodontitis had a higher incidence of peri-implantitis in comparison with periodontally healthy patients.72,73 Papantonopoulos etal.74 have reported on two implant phenotypes that are directly related to peri-implantitis. A peri-implantitis-suscep-tible phenotype was associated with fewer teeth and younger age, and was predominantly in the mandible. A peri-implantitis-resistant phe-notype was mainly found in the maxilla.74 Smoking/Tobacco UseAlthough many conicting studies exist on the relationship between smoking and peri-implantitis, most reports have shown statistically signicant dierences between smokers and non-smokers. Rinke etal.75 reported that smokers had an approxi-mate odds ratio of 31.58 in development of peri-implantitis. e overall peri-implantitis rate in their study population was 11.2% and as high as 53% for patients who smoked and had a history of periodontitis. Diabetese relationship between diabetes and periodontal disease is well established. Poorly controlled diabetes has also been associated with peri-implantitis.76,77 Venza et al.78 reported that the long-term prognosis for dental implants is more favorable when the patient’s glycosylated hemoglobin (HbA1c) is less than 7%.Canullo etal.79 proposed an evidence-based classication for dierent clinical subtypes of peri-implantitis, including: (1) sur-gically triggered peri-implantitis, (2) prosthetically driven peri-implantitis, and (3) plaque-induced peri-implantitis. ey state that these three subtypes of peri-implantitis are separate, dier-ent entities that may be distinguished with predictive proles. In addition, various risk factors can act synergistically with a clinical scenario, which make the causative factors more dicult (Table 41.2).79 PreventionHome CareAn eective oral hygiene program is paramount to minimize peri-implant disease. is has been shown through various studies. Direct correlations between poor oral hygiene and peri-implant bone loss in a 10-year follow-up study were reported.80 Other stud-ies have shown a correlation with poor oral hygiene and a higher plaque score.81 In addition, patients who have lost their teeth to periodontal disease are more susceptible to peri-implantitis.82 Professional Careorough periodontal charting and review is essential. Patients with periodontitis must have this pathologic condition controlled before implant placement. Patients who do not demonstrate the • Verticalboneloss(radiographic,probing,orboth)• Peri-Implantpockets• Bleedingonprobing• Exudate• Mucosalswelling• Erythema• Usuallynoassociatedpain • BOX 41.4 Clinical Symptoms Associated With Peri-Implantitis 1150PART VIII Dental Implant Maintenanceability to maintain oral hygiene need to be educated and put on stringent professional care regimens. Prosthetic DesignA thoroughly evaluated cone beam computed tomography scan study with favorable biomechanical design for prosthetics is man-datory. Ideal implant position is paramount to allow for a properly designed prosthesis that is cleansable. Cementation Techniquee meticulous use of cements when delivering a prosthe-sis is imperative, or the clinician can choose to use a screw-retained prostheses. If a cementable prosthesis is utilized, the clinician must take precautions to prevent retainment of cement. Conventional cementable techniques that are normally used for natural teeth are not recommended (See Fig. 41.5). ABCDE• Fig. . Peri-Implantitis. (A and B) Clinical images depicting bone loss. (C) Radiograph showing sig-nificant bone loss around implant. (D) Cratering bone loss. (E) Implant failure caused by calculus formation. 1151CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies Human Studies on Peri-Implantitis TreatmentAuthor ProcedureNumber of Patients and Implants and Time of Follow Up Treatment OutcomeLeonhardtetal2003Accesssurgery 9patients26implants60monthsSystemicantibiotics(accordingtomicro-biologicanalysis)+accesssurgery+decontaminationoftheimplantsurfaceusing10%hydrogenperoxide0.2%CHX2×adayrinseHealing:58%oftheimplants7implantslost4/19ongoingboneloss6/19bonegainMeangingivalbleedingwasreducedfrom100%–5%Diseaseprogressionat2otherimplantsRomeoetal2007Apicallyrepositionedapsurgery+implantsurfacemodicationResectivesurgery19patients38implants(11hol-lowscrewand7solidscrew)12–24–36monthsSystemicantibiotics(amoxicillinfor8days)+fullmouthdisinfection9patientswithresectivesurgeryand10withresectivesurgeryandmodicationofsurfacetopographyImplantsurfacedecontaminationwithmetronidazolegel,tetracyclinehydro-chloride,andsalineRadiographicassessment:ImplantoplastyisaneffectivetreatmentprocedureSignicantlybetterresultsw/apicalreposi-tionapsurgery+implantsurfacemodicationBehnekeetal1997Bonegraftsandbonegraftsubstitutessurgery • Nonsubmerged10patients14implants6months–2yearsIrrigationwithiodine+systemicantibiotics(Ornidazole500mg×2for7days)Implantsurfacetreatedwithairpowderandirrigationwithsaline7implantswith2–3walldefectsgotbonechipsand7implantswith1walldefectgotboneblocksClinical:(6months/14implants)BI:2.4–0.3PD:5.9–2.3mmClinical:(2years/5implants)BI:2.4–0.4PD:5.9–2.5mmRadiographic:(3–12months/14implants)Averagebonell:3mmBehnekeetal2000Bonegraftsandbonegraftsubstitutessurgery • Nonsubmerged25implants6monthsto3yearsIrrigationwithiodinefor1month+debridementwithmucoperiostealapsurgeryImplantsurfacedecontaminationwithairabrasiveinstrumentsfor30seconds+salineirrigation+7bonechipsand18boneblocks(Metronidazole400×2for7days)Clinical:(1year/18implants)PD:5.3–2.2mmClinical:(3year/10implants)PD:5.3–1.6mmRadiographic:(1year/18implants)Meanbonell:3.9mmRadiographic:(3year/10implants)Meanbonell:4.2mmAughtunetal1992Barriermembranes • Nonsubmerged12patients15implants6–12monthsePTFEmembrane+systemicantibiotics(tetracycline200mg×1for12days)+implantdetoxication(airpowder)+irrigationwithsalineClinical:PI:1.9–1.0BI:1.1–1.1PD:5.2–4.1mmRadiographicMeanboneloss:0.8mmMinorimprovementsonsofttissueconditionsMembraneexposureJovanovicetal1992Barriermembranes • Nonsubmerged7patients10implants6monthsto3yearsePTFEmembrane+systemicantibiotics(Tetracycline250mg×4for7days)+implantdetoxication(air-powder+chloramineT+salineirrigation)Clinical:PI:1.7–0.6GI:2.1–0.3PD:6.8–4.1mmAllclinicalsignsimprovedRadiographically:7defectsshowedbonell3defects:nobonellTABLE 41.1Continued 1152PART VIII Dental Implant MaintenanceAuthor ProcedureNumber of Patients and Implants and Time of Follow Up Treatment OutcomeKhouryandBuchmann2001Graftingmaterials +barrier membranes25patients41implants36monthsSystemicantibioticsGroup1(12implants):detoxicationwithchlorhexidineirrigation+citricacid+hydrogenperoxide+saline+boneblocksandparticulateboneGroup2(20implants):treatmentsasgroup1+ePTFEGroup3(9implants):treatmentsasgroup1+collagenmembrane(submerged)Clinical:1:PDreductions:5.1mm2.PDreductions:5.4mm3.PDreductions:2.61mmRadiographic:2.4mmbonell2.8mmbonell1.9mmbonell58.6%ofthebarriertreatedimplantsiteswerecompromisedbyearlyposttherapycomplicationsTheadditionalapplicationofbarriersdoesnotimprovetheoveralltreatmentoutcomes3yearsfollowingtherapyMattoutetal1995Withandwithoutgraft-ingmaterial19patients 23defects:ePTFEalone11defects:ePTFE+DFDBA+hydratedtetracyclinePostoperative:0.1%CHX+amoxicillin500mg(2×for8days)Meansuccessrate68%forthemembranegroupand90%forthemembrane+boneallograftSchwarzetal2006Graftingmaterials +barrier membranes • Nonsubmerged22patients22implants6monthsGranulationtissueremoved+implantsur-facedebridementwithplasticcurettes+irrigationwithsalineGroup1:NanocrystallineHAGroup2:Bovinexenograft+resorbablecollagenmembraneClinical:1:PD:reductions:2.1mm2.PD:reductions:2.6mm“Inbothgroups,radiologicobservationrevealedadecreasedtranslucencywithintheintrabonycomponentoftherespectiveperi-implantbonedefect.”Additionally,bothtreatmentsresultedinclinicallyreductionsinPDandgainsofCALat6monthsaftersurgerySchwarzetal2008Graftingmaterials +barrier membranes • Nonsubmerged22patients2yearsGroup1:Accessapsurgery+nanocrys-tallinehydroxyapatiteGroup2:Accessapsurgery+naturalbonemineral+collagenmembrane2patientsinNHA:severepusformationat12monthsClinically:PD:Group1:1.5±0.6mmGroup2:2.4±0.8mmCALgains:Group1:1.0±0.4mmGroup2:2.0±0.8mmBothtreatmentsshowedefcacyover2years.Naturalbonemineral+collagenmembraneshowedbetterclinicalimprovementsRoos-Jansakeretal2007aGraftingmaterials +barrier membranes • Nonsubmerged36patients65implants12monthsSystemicantibiotic(amoxicillin375×3+metronidazole400mg×2)for10daysstarting1daybeforesurgeryDebridementofthegranulationtissue,implantsurfacedecontaminationwithhydrogenperoxideandirrigatedwithsalineGroupI:Bonesubstitute+resorbablemembraneGroup2:BonesubstitutebutnomembraneGroup1:PDreduction:2.9mmMeanbonell:1.5mmGroup2:PDreduction:3.4mmMeanbonell:1.4mm Human Studies on Peri-implantitis Treatment—cont’dTABLE 41.1 1153CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesAuthor ProcedureNumber of Patients and Implants and Time of Follow Up Treatment OutcomeRoos-Jansakeretal2007bGraftingmaterials +barrier membranesSubmerged12patients16implants12monthsSystemicantibiotics(amoxicillin375×3+metronidazole400mg×2)for10daysstarting1daybeforesurgery.Debride-mentofgranulationtissue.ImplantsurfacedecontaminationwithhydrogenperoxideandirrigationwithsalineBonesubstitute+resorbablemembraneClinicalandradiographicimprovementswereobserved.PDreduction:4.2mmMeanbonell:2.3mmHaasetal2000DiodeLaser treatment duringsurgery17patients24implants3–9.5monthsImplantsurfacedecontaminationwithcurettage+laser+defectlledwithautogenousbone+ePTFEmembrane+systemicantibioticsfor5daysRadiographically:3monthsfromtimeofmembraneremoval:21.8%9.5months:meanbonegain:36.4%Bachetal2000DiodeLaser treatment duringsurgery30patients5yearsGroup1:Scaling+1.5%CHX+openapdebridement,apicalrepositioningtheap+osseousaugmentationand/ormucogingivalcorrectionsGroup2:Treatmentsasgroup1+laserdecontaminationwithdiodelaser(810nmw/6W)Group1:18months:noincreasedPD,BOPorsignofinammatoryprocess2years:2patientswithincreasePD,BOPandclinicalsignofinam-mation4years:5patientswithincreasePD,BOPandclinicalsignofinam-mationBetween3and5years:4implantsremovedGroup2:3years:norelapse5years:5patientswithincreasePDandclinicalsignsofinammationNoimplantremovedSignicantreductionofgram-negative,anaerobicbacteriainlasergroupthanconventionalgroupDortbudaketal2001Diodelaser treatment duringsurgery15patients15implantsImplantsurface:Curettage+rinsingwithsalinefor1minute,thenstainedwithtoluidineHalfoftheimplantsfurthertreatedwithdiodelaserfor1minuteTBOaloneresultsinasignicantbacterialreductionofP. intermediaandAAonplasmaame-sprayedcontaminatedimplantsurfaces,whileacombinedtreatmentleadstoareductiontoAA, P. gingivalis,andP. intermedia. CompleteeliminationofbacteriawasnotachievedRomanosandNentwig2008CO2laser+boneaugmentation+membrane15patients27.10±17.83monthsOpenapdebridementw/titaniumcurettes+CO2laser(2.84±0.83watts)for1minuteBoneaugmentation(bovineorautogenousbone)andcollagenmembraneNosystemicantibioticsPI:Preoperative:1.01±1.37Postoperative:0.98±1.20BI:Preoperative:2.76±0.35Postoperative:1.03±0.85PD:Preoperative:6.00±2.03mmPostoperative:2.48±0.63mmKeratinizedtissueBI:Preop:2.30±1.45mmPostop:2.41±1.39mm Human Studies on Peri-implantitis Treatment—cont’dTABLE 41.1Continued 1154PART VIII Dental Implant MaintenanceAuthor ProcedureNumber of Patients and Implants and Time of Follow Up Treatment OutcomeDeppeetal2007CO2laser+boneaugmentation32patients73implants4monthsand5yearsGroup1(19implants):Softtissueresection+conventionaldecontaminationGroup2(15implants):Treatmentasgroup1+βTCP+autogenousbonegraftsGroup3(22implants):Softtissueresection+CO2laserdecontaminationGroup4(17implants):Treatmentasgroup3+βTCP+autogenousbone3implantslostingroup14implantslostingroup22implantslostingroup34implantslostingroup4BeginningofhygienephasePI:Group1:1.8±1.2Group2:1.4±1.2Group3:1.4±0.9Group4:2.6±0.5BI:Group1:2.7±0.9Group2:2.3±1.4Group3:2.8±1.2Group4:3.3±0.6PD:Group1:6.2±1.8Group2:5.1±1.7Group3:5.7±1.4Group4:5.7±1.4ImmediatelybeforesurgeryPI:Group1:0.7±0.8Group2:0.9±0.4Group3:0.7±0.8Group4:0.5±0.6BI:Group1:0.7±0.8Group2:0.5±0.8Group3:0.6±0.3Group4:1.2±0.6PD:Group1:5.1±1.3Group2:4.8±1.4Group3:6.1±1.6Group4:5.0±1.34monthsPI:Group1:0.6±0.7Group2:0.6±0.6Group3:0.8±0.6Group4:0.5±0.4BI:Group1:0.9±0.5Group2:0.6±0.6Group3:0.7±0.6Group4:0.9±0.8PD:Group1:3.2±0.9Group2:2.4±0.7Group3:2.1±1.3Group4:1.0±0.75years Human Studies on Peri-implantitis Treatment—cont’dTABLE 41.1 1155CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesAuthor ProcedureNumber of Patients and Implants and Time of Follow Up Treatment OutcomePI:Group1:0.8±0.8Group2:1.1±0.8Group3:1.0±1.3Group4:1.2±1.3BI:Group1:1.1±1.2Group2:2.1±1.4Group3:1.8±1.1Group4:1.9±1.0PD:Group1:4.3±1.2Group2:2.5±1.1Group3:3.4±1.5Group4:2.5±1.4Treatmentofperi-implantitismaybeac-celeratedbyusingaCO2laser+softtissueresectionLong-termresultsinaugmenteddefects,nodifferencebetweenlaserandconventionaldecontaminationFroumetal2012RegenerativeapproachBiologics+bone+membrane51implants38patients3–7.5yearsSystemicantibiotics(2000mgamoxicillinor600mgclindamycin)1hrbeforesurgeryandcontinue500mgamoxicil-lintidorclindamycin150mgqidforadditional10daysSurfacedecontaminationw/bicarbonatepowderfor60seconds(airabrasivedevice),60-secondirrigationwithster-ilesaline,tetracycline(50mg/mLwithcottonpelletsorbrushfor30seconds,thensecondbicarbonateairabrasion60seconds,applicationof0.12%CHXfor30seconds,then60secondsreirrigationwithsterilesaline+enamelmatrixderivatives+anorganicbovinebonesoakedinplateletderivedgrowthfactorforatleast5minutesormin-eralizedfreeze-driedbone+collagenmembraneorsubepithelialCTgraftatarea(<2mmKG)Group1:Greatestdefectdepthradiographi-callyGroup2:Greatestbonelossonthefacialofimplant•Noimplantlost•PDreduction:Group1:5.4mmGroup2:5.1mm•Bonelevelgain:Group1:3.75mmGroup2:3mmAA, Aggregatibacter actinomycetemcomitans; BI, Bleeding index; BOP, Bleeding on probing; BTCP, Beta Tricalcium Phosphate; CAL, Clinical attachment level; CHX, Chlorhexidine; DFDBA, Demineralized freeze-dried bone allograft; ePTFE, expanded polytetrafluoroethylene; GI, Gingival Index; HA, Hydroxyapatite; KG, Keratinized gingiva; NHA, Nanocrystalline Hydroxyapatite; PD, Probing depth; PI, Plaque index; TBO, toluidine-blue-O.From Suzuki JB, Misch CE. Periodontal and maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implantology. St. Louis, MO: Elsevier; 2018. Human Studies on Peri-implantitis Treatment—cont’dTABLE 41.1Control of Parafunctional ForcesAn occlusal guard is crucial in preventing unfavorable occlusal stress. e night guard is adjusted to be on a at plane occlusion to disperse stress. Careful discussion should be conducted with the dental laboratory to convey the desired design for successful clinical outcomes. Managemente objective of treatment for peri-implantitis is for osseous regen-eration of the implant-bone defect. However, such treatment has been challenging because the implant surface needs to be detoxi-ed, along with modifying the soft and hard tissues. is may involve nonsurgical and surgical treatment. 1156PART VIII Dental Implant MaintenanceNonsurgical Management of Peri-ImplantitisNonsurgical treatment of peri-implant mucositis is often success-ful. In contrast, the nonsurgical treatment for peri-implantitis is not as predictable. is is most likely due to the inability to remove the bacterial biolm from the exposed implant surface. Such diculty has been especially observed with rough surface dental implants.83 A systematic review illustrated that implant surfaces and diameter are potential risk factors for bone loss and peri-implantitis.84e nonsurgical treatment of peri-implantitis usually involves the debridement and detoxication of implant surfaces, similar to the treatment of peri-implant mucositis. However, the issue that arises is that these exposed surfaces usually have concurrent sub-gingival pockets.Low-Abrasive Amino Acid Glycine Powder. Low-abrasive amino acid glycine powder has been shown to be an eective treat-ment for removing biolm without damaging the implant surface, and hard and soft tissues of the periodontium. is technique uses a special handpiece with a plastic tube nozzle with three orthogo-nally oriented holes. An air-powder mixture with reduced pressure is expelled through the nozzle, which prevents the formation of air emphysema complications. e nozzle is moved in a circumferen-tial movement around the implant surface.85Although more extensive studies need to be conducted as to technique ecacy, glycine powder can be incorporated into a treatment regimen. e clinician should be careful to use the pow-der only in areas where access is available, including a posttreat-ment rinse to remove any residue. is modality is best used in cases with a buccal dehiscence and/or horizontal bone loss with-out crater or infrabony pocketing. An air-powder unit (Hu-Friedy, Chicago, Ill.) that adapts to a slow-speed handpiece is available and may be used eectively (Fig. 41.10). Ultrasonic Devices. For treatment of peri-implantitis, tip modications (i.e., carbon ber, silicone, or plastic) must be used. Care must be exercised not to use metal tips as they may alter the implant surface. Ultrasonic devices should be used only when plastic tips are available. Irrigation and meticulous cleaning are recommended in treatment for either open ap debridement or closed ap irrigation. Lasers. One of the newer and least invasive methodologies to treat peri-implant mucositis and peri-implantitis involves the use of laser photonic energy, a coherent form of infrared or visible light, usually of a single wavelength. Lasers have been used eec-tively for decades in oral implantology in second-stage recovery of implants through the ablation and vaporization of overlying soft tissue.86Laser Protocols. Similar to their use in treating periodontal disease, lasers provide dierent treatment approaches for peri-implantitis: nonsurgical, surgical, antimicrobial photodynamic therapy, and photobiomodulation.•  Nonsurgical: In the nonsurgical modality, lasers are used adjunctively to help remove calculus, reduce inammation and remove diseased soft tissue, and reduce subgingival pathogens. Using dierent types of lasers, such as the diode, Nd:YAG (neodymium-doped yttrium aluminum garnet), erbium, or carbon dioxide laser, the laser beam is directed at the inamed soft tissue within the sulcus, using noncontact overlapping strokes to disrupt the biolm, reduce the microbial popula-tion, and decontaminate the pocket epithelium. Erbium lasers have also been shown to remove calculus from the implant surface.87-95•  Surgical: Minimally invasive laser-assisted surgical techniques involve removal of diseased epithelial lining. More invasive surgical procedures involve conventional elevation of a full-thickness ap for surgical access, followed by laser-assisted degranulation, surface debridement and decontamination, and osseous tissue removal or recontouring. As indicated, bone augmentation may be performed through placement of bone-grafting material.96-103•  Antimicrobial Photodynamic erapy: Antimicrobial photody-namic therapy in periodontology is a light-based approach to ter-minating bacteria. A photoactivatable substance (photosensitizer) is applied to the targeted area (i.e., within the sulcus) and then activated by laser light. Singlet oxygen and other cytotoxic reac-tive agents are produced to reduce periodontopathogens.104-109•  Photobiomodulation: is a form of light therapy that uses non-ionizing forms of light, including lasers in the visible and infrared spectrum. e nonthermal technique is used to elicit photophysical and photochemical events. In implantology, it is used to promote wound healing and tissue regeneration. It has also been shown to increase osteoblastic proliferation, collagen deposition, and bone neoformation.110-115Although laser-based peri-implantitis treatment techniques are generally positive, some studies indicate adjunctive use of lasers have limited or no extra benecial eect compared with conventional treatment methodologies. Additional well-designed, long-term, randomized controlled trials are needed to verify the clinical and microbiologic outcomes of laser use.116-118Assurance of positive therapeutic outcomes is facilitated by an informed clinical technique, prudent use of proper laser operating parameters, and awareness of all laser wavelengths. However, when used inappropriately, laser energy can adversely alter implant sur-faces and/or induce undesirable temperature increases, which may be detrimental to implant health119-122 (Fig. 41.11).In 2014 a human clinical study consisting of 16 patients was published, using a pulsed 1064-nm Nd:YAG laser (PerioLase MVP-7; Millennium Dental Technologies, Cerritos, Calif.). e technique introduced is known as the Laser-Assisted Peri-Implan-titis Protocol (LAPIP) to manage patients with peri-implantitis123 without the use of bone augmentation (Fig. 41.12). (LAPIP is Predictive Proles Associated With Peri-Implantitis223,224Risk Factor Predictive ProfilesType 1:surgicalfactors • Presenceofplaqueassociatedwithorovestibularandmesiodistalimplantmalpositioning• FailedbonereconstructionType 2:prostheticfactors• Plaqueassociatedwithretainedcementremnants• Nonidealnishlinemargin(≥2mmbelowsofttissuemargin)• Occlusaloverloading• Prosthesismaterialfracture• Abutmentscrewloosening• ImplantfractureType 3:plaque-induced Generalizedbone-levelrecessionassociatedwithplaqueaccumulation,withoutanysurgical/prostheticcomplication TABLE 41.2 1157CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapiesa registered trademark of Millennium Dental Technologies, Inc., Cerritos, Calif.)e clinicians used a modication of a well-dened surgical pro-cedure, the Laser-Assisted New Attachment Protocol (LANAP), used for treating periodontitis. is technique was dened as a minimally invasive surgical therapy that may be appropriate for multiple periodontal defects and possibly as a rst line of manage-ment of periodontal disease.124 In two recent histologic studies, the LANAP has shown evidence of new attachment and tissue regeneration.125,126 Based on this evidence, in 2016 the U.S. Food and Drug Administration granted marketing clearance for the PerioLase MVP-7 Laser for a rst-of-its-kind clinical indication for use: periodontal regeneration, that is, true regeneration of the attachment apparatus (new cementum, new periodontal ligament, and new alveolar bone) on a previously diseased root surface when used specically in the LANAP.For the treatment of peri-implantitis, the LAPIP follows the step-by-step sequence dened in the LANAP procedure, but with a reduced light dose (energy) around implants. 1. Surgical probings are performed under local anesthesia to record the depths of all bony defects around the implant. Pocket depth and phenotype help to determine the amount of laser energy to be delivered during the ablation and hemostasis applications. 2. e laser ber is then inserted into the periodontal pocket, oriented in a prescribed fashion, and the laser is activated at particular settings to ablate (remove) the diseased epithelial lin-ing and granulomatous tissue, to denature pathologic proteins, and to create bacteria antisepsis. 3. Ultrasonic scalers are used to remove foreign substances (including calculus and cement) from the implant surfaces. 4. Bone is modied, removed, reshaped, and decorticated in a prescribed manner to stimulate the release of blood, stem cells, and growth factors from the bone. 5. e laser is then used again at specically adjusted settings in hemostasis mode to form a thick, stable brin clot, activate growth factors, and upregulate gene expression. 6. Coronal soft tissue is approximated against the implant using nger pressure to achieve adhesion. No sutures are used because this is a apless procedure. 7. Removal of occlusal interference is performed to reduce trau-matic forces and mobility.e technique has been shown to produce healing in an envi-ronment conducive to true regeneration of new alveolar bone. Reosseointegration of the implant is anticipated.e study analyzed 16 cases, 9 females and 7 males, with an average age of 54 years and a range of 32 to 79 years. Median time that had elapsed between the date of implant placement and the date of LAPIP treatment was 4 years (3 months to 16 years). Follow-up data ranged from 8 to 36 months after LAPIP treat-ment. All clinicians reported control of the peri-implantitis infec-tion, reversal of bone loss, and rescue of the incumbent implant.Radiographic evidence combined with three-dimensional geo-metric modeling was used to estimate the rate of addition of new bone to the alveolar crest. e rate of bone deposition was deter-mined to be 14.9 mm2 in cross-sectional area per year. In two cases, new bone deposition was observed at rates of 0.62 and 1.6 mm3 per month, respectively. Complete recovery (resolution of AC DBE• Fig. . (A) Low-Abrasive Powder. Hu-Friedy glycine powder jet used to debride titanium implant surfaces, (B) Titanium Brushes, (C) Clinical image of titanium brushes applying detioxification agent, (D) Implantplasty Kit for removal of implant threads, (E) Implant with threads removed. 1158PART VIII Dental Implant MaintenanceABCD• Fig. . Laser Treatment. (A) Initial evaluation of peri-implantitis. (B) Laser tip activated around sulcular margins of implant. (C) Immediate postsurgical appearance. (D) Two weeks postoperatively with granula-tion tissue re-forming around implant collar. (From Suzuki JB, Misch CE. Periodontal and maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implantology. St. Louis, MO: Elsevier; 2018.)ABCDEFGH• Fig. . Artists sketch of sequence of clinical steps for Laser-Assisted Peri-Implantitis Protocol (LAPIP) procedure using the PerioLase MVP-7 pulsed neodymium-Yttrium Aluminum garnet (Nd:YAG) laser. (per-mission from Millenium, Cerritos, CA USA and From Suzuki JB. Salvaging implants with an Nd:YAG laser: a novel approach to a growing problem. Compend Contin Educ Dent. 2015;36:756-761.) 1159CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapiesperi-implantitis) averaged 1 to 3 years, depending on the size of the initial lesion. Analysis of collected data revealed that bone deposition is not linear. Large defects healed more rapidly at rst, but the rate slowed as the defect diminished. A modest trend was shown for larger lesions to heal more rapidly.Although the results of this clinical study appear promising, further study of the predictability and eectiveness of the LAPIP technique is warranted. e eectiveness of the 1064-nm Nd:YAG laser wavelength in achieving its successful clinical outcomes with the LAPIP protocol may be attributed to a variety of factors.127 ese include the Nd:YAG laser’s ability to:• selectivelyremoveinamedpocketepithelium,withnosigni-cant damage to underlying connective tissue,128-131• reduce pathogenic microorganisms in the periodontalpocket,132-136• produceanantiinammatoryeect,137-140 and• stimulatealveolarbonegrowthatthecellularlevel.141-144Whether used adjunctively or as the primary instrument, lasers oer the eld of oral implantology a number of safe and eec-tive clinical applications for the treatment of peri-implant muco-sitis and peri-implantitis. Techniques range from nonsurgical and surgical uses, to antimicrobial photodynamic therapy and photo biostimulation. Additional investigations will further determine the underlying mechanisms of their action. Proper training and scrupulous adherence to specic laser-based protocols will help assure favorable therapeutic patient outcomes.Laser settings are specic to each individual laser according to manufacturers’ protocols. Care should be exercised to cover all exposed surfaces (i.e., each exposed thread) for the detoxication process. Use of regenerative material (allografts and extended resorb-able membranes) is highly recommended. Tissues are modied and sutured to reapproximate tissue for tension-free primary closure.It is critical to limit time exposure of the implant surface with the laser application to avoid overheating or charring. is may increase implant morbidity and possibly lead to premature loss of the implant because of bone disintegration.Locally Applied Antibiotics. e recommended locally applied antibiotic (LDA) during surgical implant rescue is tetracycline at 50 mg/mL solution. Tetracycline capsules can be opened and mixed with small amounts of saline solution to create a paste. is paste is burnished onto implant surfaces for 60 seconds, then thoroughly rinsed with saline. Tetracycline is bacteriostatic, as it targets the 30s ribosomal subunit in the messenger RNA translation complex of bac-terial protein synthesis. Because tetracycline has an inhibitory eect on matrix metalloproteinases, the tetracycline paste needs to be com-pletely removed. A study with pure tetracycline application showed reosseointegration after 4 months.56 It is highly recommended to incorporate tetracycline in surgical rescue therapy for peri-implantitis.Tetracycline capsules (two 500-mg capsules) may be mixed with a few drops of saline to form a viscous consistency. It should stay gelled when applied to exposed implant surfaces during sur-gery. e mixture is allowed to sit on the implant surface for 1 minute, then is thoroughly rinsed o. It allows proximal contact of antibiotics to implant surface colonies and may assist in success in treatment of peri-implantitis.Another option of local antibiotic administration is with mino-cycline, which is a tetracycline derivative. Minocycline is manu-factured in an encapsulated microsphere of poly(lactic-coglycolic acid), a biodegradable polymer called Arestin (OraPharma, Warm-inster, Pa.).57 e subgingival application of minocycline micro-spheres has been shown to maintain therapeutic levels for 14 days. Williams etal.58 reported on a 9-month study that showed the therapeutic ecacy of minocycline microspheres in signicantly reducing probing depth in conjunction with scaling. Oringer etal.59 concluded that minocycline microspheres induce a potent short-term reduction in the gingival crevicular uid molecular markers of bone resorption (Fig. 41.8). Systemic Antibiotics. e use of systemic antibiotics has been established for management of periodontitis.60 However, peri-mucositis treatment studies with use of systemic antibiotics are lacking. It is known that patients with periodontitis are three times more likely to experience peri-implantitis, but the bacte-rial colonies found in peri-implantitis and periodontitis share few characteristics. Still, many studies have demonstrated the most eective antibiotic combination is amoxicillin and metronidazole.Metronidazole is bactericidal to anaerobic organisms and disrupts DNA synthesis. It has been shown to be especially eective against A. actinomycetemcomitans, P. gingivalis, and P. intermedia.61 e combi-nation of amoxicillin and metronidazole has also been shown to have long-term eects against A. actinomycetemcomitans62 (Box 41.3).For patients who are allergic to amoxicillin, alternative systemic antibiotics are clindamycin, ciprooxacin, metronidazole, or azithro-mycin. Local drug delivery systems such as minocycline (Arestin, o U.S. Food and Drug Administration label) may be considered. Surgical Management of Peri-ImplantitisAlthough nonsurgical treatment of peri-implantitis may be eective in some cases, the majority of cases require a more inva-sive approach to ensure an eective treatment outcome. ere are various surgical techniques (see later) to treat peri-implan-titis, depending on the nal objective.145 Surgical management is completed with curettes, specialized titanium brushes with an implant handpiece, and/or a glycine polishing handpiece. Along with mechanical decontamination, a chemical decon-tamination process should be followed, using compounds such as doxycycline/tetracycline or citric acid. e aps are then • Fig. . Locally Applied Antibiotic. Arestin placed into the sulcus area for the treatment of peri-mucositis.Amoxicillin500mgtid(threetimesperday),totalof21capsulesMetronidazole250mg,21tabletstid,untilallconsumedbythepatientMinocycline(Arestin)appliedsubgingivallyaroundimplantswithpockets • BOX 41.3 Antibiotic Prescription Formulation 1160PART VIII Dental Implant Maintenancereapproximated in their original position, using horizontal mattress sutures, which adapt tissue around the implant while creating a ferrule eect. Interrupted sutures will also serve this purpose (Fig. 41.13).It is possible to also complete a subepithelial tissue augmenta-tion while performing the access ap debridement. Simultaneous tissue grafting with debridement had a signicant reduction of bleeding on probing, pocket depth, and clinical attachment loss at a 6-month postoperative evaluation.146 1. Sulcular incision around desired dentition being careful to extend at least one tooth mesial and one tooth distal in antici-pation to the area of treatment 2. Full-thickness ap reection is complete past the mucogingival junction on both buccal and palatal/lingual if necessary 3. Implants are detoxied with tetracycline paste, EDTA, or citric acid, cleaned with curettes and titanium brushes 4. Air powder glycine to further clean implant threads previously exposedABCDE• Fig. . Peri-implantitis Treatment. (A) Clinical view of localized edematous tissue. (B) Radiograph depicting circumferential bone loss. (C) Three months post-LANAP treatment. (D and E) Nine months post-LANAP treatment. (Courtesy Allen Honigman, DDS) 1161CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies 5. Flaps are readapted over osseous structure and should be in relatively similar position 6. Horizontal mattress sutures or interrupted sutures may be used, being cautious not to exert excess tension, which causes bunching of tissues; tissue does not have to be completely approximated; new tissue will form and granulate in the wound siteHeitz-Mayeld et al.147 reported on a 12-month prospec-tive study with antiinfective surgical therapy outcomes for peri-implant disease. irty-six patients with moderate to advanced peri-implantitis had access ap disinfection, followed with a com-bination of systemic antibiotics (amoxicillin and metronidazole). At 1 year, 92% of patients had stable crestal bone height, and all had a marked reduction of probing depth. On probing, 47% had complete resolution of bleeding.147Regenerative Procedures. For peri-implantitis cases where a crater-like defect is present, regeneration is recommended (Fig. 41.14). Even though regeneration is an ideal treatment modality for all peri-implantitis cases, there are criteria that must be ful-lled to allow successful treatment. In a similar principle to bone ABCDE• Fig. . Regenerative Procedures. (A) Radiograph depicting significant bone loss surrounding implant in the first molar position. (B) Full-thickness reflection showing extent of defect with retained cement. (C) Detoxification with tetracycline hydrochloride, after removal of cement. (D) Augmentation with allograft. (E) Postoperative radiograph 2 years postoperatively. (Courtesy Dr. Nolen Levine.) 1162PART VIII Dental Implant Maintenanceregeneration for natural teeth, the greater number of osseous walls remaining in a defect, the better the anticipated clinical outcomes.Also, the prosthesis must be free from any premature contacts that may introduce excessive force to the implant interface. Ide-ally, especially in single-tooth implant cases, removal of the crown would be performed to ensure proper healing. A sulcular incision is performed from one tooth mesial to one tooth distal of the implant. A full-thickness mucoperiosteal ap is reected to gain adequate access to defect. orough removal of granulation tis-sue is vital. Mechanical debridement is then initiated. A titanium brush with a small tip may be needed to access the implant surface if the osseous crater around the implant has little access.After thorough mechanical debridement, freeze-dried bone allograft may be packed in with a resorbable membrane. Soft tis-sue augmentation may also be included, which will enhance heal-ing. Flap advancement is usually indicated to achieve soft tissue primary closure around implants. A high tensile suture material suture is recommended to ensure the ap does not open prema-turely. Implants should be free from any pressure or premature contacts that may introduce excessive force to the implant inter-face. Ideally, especially in single-tooth implant cases, any occlusal prematurities should be removed.In addition to the steps listed earlier, enamel matrix protein, platelet-derived growth factor, and human allograft or bovine xeno-graft in conjunction with a collagen membrane or subepithelial tis-sue graft was suggested to enhance regeneration. Systematic reviews on the merits of clinical regeneration, of platelet concentrates148 and bone marrow aspirates have been published recently.149 Regenerative Technique 1. Sulcular incision is made around the clinical site with one tooth mesial and one tooth distal. 2. Full-thickness mucoperiosteal ap is reected past the mucogin-gival junction to ensure enough tension release from ap tissue. It is essential to produce adequate release so there is minimal tension when closing the ap. Inadequate reection will result in incision line opening, which will increase morbidity of the graft. 3. e bone surface is curetted to clean and remove all soft tissue remnants. Bone surface is curetted, being careful to remove all remnants of soft tissue. Detoxication: a. Tetracycline paste, EDTA, or citric acid is applied to the exposed surface for 30 to 60 seconds. b. Rinse with sterile saline for 30 seconds. 4. A full-thickness ap is reected to gain adequate access to the defect and implant threads. orough removal of granulation tissue is critical. Bone graft of choice (i.e., ideally an autograft or allograft) is placed on defect. 5. A resorbable membrane (extended resorbable collagen mem-brane: 4–6 months) is then draped over bone graft, being care-ful to cover 3 mm past all edges of bone graft. 6. Tissue tension is reduced via tissue-stretching techniques. Flaps are sutured (i.e., high-tensile strength suture material [polygly-colic acid (PGA) sutures, 4–0]), being careful to provide ten-sion-free closure to produce maximal contact between tissue edges (primary closure) (Fig. 41.15). Apically Repositioned Surgical Technique. is surgical technique is used for implants that have generalized horizontal bone loss greater than one to two threads. An internal bevel inci-sion or sulcular incisions circumscribing buccal and lingual con-tours of the implant are made. Two vertical incisions are added on the mesial and distal of the implant, creating a pyramidal ap. e clinician should recognize the importance of the blood sup-ply of the ap, and a wide base is necessary to ensure the sulcular margin of the ap does not slough. On the lingual/palatal a gin-givectomy may be performed at the level of the anticipated nal gingival height. Submarginal incisions may be performed in cases where keratinized gingival tissue is adequate (e.g., palate). Ideally a partial-thickness ap is recommended because it will improve api-cal ap adaptation. Full-thickness aps elevation technique may be easier in dicult-to-access clinical sites.Once reected, similar treatment as the access ap may be vital. Granulation tissue needs to be completely removed, followed by thorough cleaning of implant surfaces. A chemical detoxication can similarly be performed. A decision may be made to remove implant threads with a handpiece if signicant loss of osseous support is present and regeneration is unlikely. e nal ap is sutured to the underlying periosteal tissue if a split-thickness ap was used. If a full-thickness ap was performed, it can be adapted apically via individual interrupted sutures. e goal is to readapt tissue back onto remaining osseous support to minimize thick-ness of a soft tissue collar, thereby minimizing probing depth.Steps of Flap Access, Debridement, and Resective Surgery are described below: 1. Sulcular incision is made around desired dentition, being care-ful to extend at least one tooth mesial and one tooth distal in anticipation to the area of treatment. 2. Full-thickness ap reection is complete past the mucogingival junction on both buccal and palatal/lingual if necessary. 3. Osseous recontouring is complete at this time to create a posi-tive architecture. 4. Implants are detoxied with tetracycline paste, EDTA, or citric acid, cleaned with curettes and titanium brushes. 5. Air-powder glycine treatment of exposed implant threads is performed. 6. Flaps are readapted over remaining osseous structure and should be apical in comparison with the original ap position. 7. Horizontal mattress sutures or interrupted sutures can be used, being careful not to exert too much tension that causes bunch-ing of tissues. Tissues do not have to be completely approximated. New tissue will form and granulate in the wound site (Table 41.3). Platelet Concentrate Growth Factors. In implant dentistry the two most common platelet concentrates are termed under the general acronyms of PRP (platelet-rich plasma) or PRF (platelet-rich brin). ese products are often considered growth factors and used in regenerative medicine. Although protocols vary, most platelet concentrates are blood extracts from a whole blood sample that is processed via centrifugation. e processing technique sep-arates the blood components into usable (e.g., brinogen/brin, platelets, growth factors, and leukocytes in liquid plasma) or unus-able (e.g., red blood cells).150e use of platelet concentrates (e.g., PRP and PRF) for the treatment of peri-implant defects has been widely researched, with varying results. Unfortunately, the literature on this topic is con-troversial and conclusions are extremely variable.Platelet-Rich Plasma. PRP with and without bone substitutes has been studied with the treatment of peri-implant defects. In various dog research models, most researchers have not found ben-ecial results with PRP alone,151 in combination with xenograft bone,152-154 and with guided bone regeneration procedures.155 In general the literature as a whole has not shown a signicant benet in the treatment of peri-implant defects. Simonpieri etal.,156 in a comprehensive review, stated that PRP does not show conclusive results. A possible reason for this is that natural bleeding from the surgery site is sucient to saturate the area with blood growth fac-tors and allow for increased healing ability.  1163CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesABCED• Fig. . Treatment of Peri-implantitis. (A) Maxillary right canine exhibiting bone loss and peri-implantitis. (B) Clinical view. (C) Full-thickness reflection depicting the circumferential and buccal bone loss. (D) Lingual view of defect and thread removal. (E) Removal of soft tissue remnants with titanium brush. 1164PART VIII Dental Implant MaintenanceHGFIJKLMFig. ., cont’d (F) Citric acid powder mixed with saline. (G) Citric acid applied to implant surface for detoxification. (H) Irrigation with saline. (I) Tetracycline paste. (J) Tetracycline mixed with saline. (K) Tetracy-cline paste applied to implant surface. (L) Irrigation with saline. (M) Tissue tension evaluated. 1165CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesP QONFig. ., cont’d (N) Decortication. (O) Confirmation of bleeding from cortical holes. (P) Acellular dermis modified and placed with tacks. (Q) Autograft harvested from tuberosity. 1166PART VIII Dental Implant MaintenancePlatelet-Rich Fibrin. In contrast, PRF is used as a “generic” name for the second-generation platelet concentrates, which are derivatives of PRP. e original protocol by Dohan, Choukroun, etal.157 used no anticoagulants and was termed L-PRF (leuko-cyte- and platelet-rich brin). Later, they have been modied to include advanced-PRF (A-PRF) and injectable-PRF (i-PRF), as well as several other groups of products.e L-PRF brin matrix contains mostly platelets and leu-kocytes (e.g., lymphocytes). e L-PRF clot is created without blood modication (i.e., no anticoagulants) and is the result of the natural coagulation process during centrifugation.158 Because of its strong brin network and bone growth cell factors (leukocytes, platelet aggregates, circulating stem cells), the L-PRF clot has been shown to have benecial results, with bone substitutes in the ll-ing of peri-implant defects.With respect to bone regeneration and treatment of defects, L-PRF has been shown to be benecial when added to bone substitute material.159 Also, when L-PRF is used as a regener-ated membrane, increase soft tissue healing is seen. Numerous studies have conrmed increased benets of soft tissue stimula-tion and promotion of gingival remodeling.160,161 e L-PRF has also been shown to regulate the interactions between the bone and soft tissue, thereby promoting healing and remodeling of the tissue.162Because peri-implantitis involves an inammatory and bac-teria-laden defect, the exposed implant surface is contaminated with a bacterial biolm and altered surface characteristics. e titanium oxide surface is destroyed with peri-implant disease, new bone growth can be initiated only after complete decon-tamination of the implant surface. erefore, if the contami-nated surface is not restored, bone grafting will most likely not be successful. Multiple protocols have been suggested to clean (i.e., detoxify) the implant surface. Although dependent on the type of implant surface, the use of PRF in the bone regeneration technique has been shown to heal compromised peri-implant defects.163 Protocol. 1. A full-thickness reection is completed to expose the osse-ous and mucogingival defect. Debridement is completed to remove nonvital hard tissue, together with granulation tissue. 2. e implant surface is then detoxied with citric acid, EDTA, and/or tetracycline paste. A titanium brush may be used with a latch-type handpiece to aid in the decontamina-tion process. 3. A whole blood sample is collected in a 10-mL tube without an anticoagulant. 4. e blood sample is immediately centrifuged for 12 minutes at approximately 2700 rpm. Because there is no anticoagulant, the platelets are activated and trigger the coagulation cascade when they contact the tube walls. ere will exist three distinct layers: (1) top layer—platelet-poor plasma (PPP); (2) middle layer—PRF; and (3) bottom layer—red blood cells. 5. e brinogen is transformed into a brin network via the cir-culating thrombin. e resultant brin clot is located in the center of the tube, which is concentrated with acellular plasma and platelets.R STUVFig. ., cont’d (R) Autograft placed as first layer. (S) Allograft placed as second layer. (T) PRF membrane placed over acellular dermis. (U) Platelet-rich fibrin syringed under flap. (V) Final closure. 1167CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapies Treatment of Peri-mucositis and Peri-implantitisTABLE 41.3Peri-MucositisPatient Self-AdministeredPlaque Control• Toothbrushes(manualorpowered)• Toothpastes• Antimicrobialrinses• Flossing/oralirrigators• Topicalapplicationofgel• Systemicantibiotics• ProbioticLactobacillus reuteri–containingtabletsProfessionalMechanicalplaquecontrol • Handinstruments • PoweredinstrumentsChemicalplaquecontrol • Localdeliveryofantibiotics • Chlorhexidine(antimicrobials) • Phosphoricacid • Ozone,oxygen,andsalinesolutionMucogingivaldebridementProsthesisalterationPeri-ImplantitisNon-SurgicalMechanicalinstruments • Nonmetalinstruments • Rubbercups • Airabrasive • Metalinstruments • BursAdjunctivetreatments • Microbiologictest • Localantimicrobials • SystemicantimicrobialsDisinfecttitaniumsurfaces • Antiseptics • Chemical • Airpolishing • LaserMucogingivaldebridementProsthesisalterationSurgical• Openapdebridement• Surfacedecontamination• Regenerativeapproaches• Biologics• Guidedtissueregeneration• Guidedboneregeneration• SystemicantibioticsRetrograde Peri-implantitis (Maintenance and Prevention)Patientself-administeredpreventiveregimensSupportiveperiodontaltherapy/maintenance(professionally)• Mechanicalnonsurgicaltherapy • MucogingivalDebridement • ProsthesisAlterationAdapted from Suzuki JB, Misch CE. Periodontal and maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implantology. St. Louis, MO: Elsevier; 2018. 6. e acellular plasma (PPP), which is the top layer, may be removed with a pipette into a syringe. e PRF brin clot is then placed into a PRF box and processed into a membrane. e liquid part (PRF) of the PRF box is then collected and placed in with the graft material. If additional liquid is indicated for the graft material, the acellular plasma (PPP) may be added, as a small number of platelets are present in this concentrate. 7. After grafting the defect, the PRF membrane is placed over the defect. If a second membrane is used (e.g., collagen), then the membrane may be moistened with acellular plasma. 8. e soft tissue aps are approximated and closed with a high-tensile-strength suture material (e.g., Vicryl, polytetrauoro-ethylene [PTFE]).In conclusion, the L-PRF technique is a simple, eective, and nonexpensive technique to enhance the soft and hard tissues around peri-implant defects. When added to the bone substitute material, there exist immune and antibacterial properties that ben-et the healing process.164,165 e use of L-PRF as a membrane allows the peri-implant defect to create a healthy, thick, and stable soft tissue interface for increased soft tissue health. Suzuki-Resnik Peri-Implant Disease ProtocolTo simplify the treatment of peri-implant disease and maintenance protocols, Suzuki and Resnik have formulated a comprehensive treatment regimen. is consists of four protocols with associated detailed step-by-step regimen.PROTOCOL 1:< 3mm probing depthsNo Plaque or No Bleeding on Probing (BOP)Treatment• MaintainRegularHomeCare• 3-6monthhygienerecall PROTOCOL 2: (Peri-Implant Mucositis)< 3mm probing depthsPlaque presence / Bleeding on Probing (BOP) Or 3 – 5 mm probing depthsPlaque presence / Bleeding on Probing (BOP)Treatment• FollowTreatment Regimen A• IncreaseHygieneRecallFrequency(∼ 3 months)• IncreaseHomeCareEducation• Ifnoresolution,proceedtoProtocol3  1168PART VIII Dental Implant MaintenancePROTOCOL 3: (Peri-Implantitis)> 5 mm probing depthsPlaque presence / Bleeding on ProbingCrestal Bone Loss > 2 mmTreatment• FollowTreatment Regimen A, B, C, & D• IncreaseHygieneRecallFrequency(∼ 3 months)• IncreaseHomeCareEducation• Rx PROTOCOL 4: Implant MobilityPain upon functionBone loss > 50% of implant lengthUncontrolled exudateTreatment• FollowTreatment Regimen E Peri-Implant Disease Treatment RegimenTreatment Regimen A: Mechanical Closed Debridement (Acceptable Instrumentation)• Resin, Titanium, Graphite, Carbon-Fiber, and Gold-tippedinstruments can be used to remove deposits• ProphyCup/Brush• Air-Polisher with Glycine Powder (Hu-Friedy), Prophy Jet(Dentsply)• Cavitron(useblueimplanttip)• Rx:Chlorhexidine(0.12%,0.2%)orcetylpyridiniumchloride• CheckOcclusion Treatment Regimen B: Antiseptic Therapy• Subgingivalantisepticirrigation(0.12%,0.2%Chlorhexidine)is added to the mechanical therapy ○ Irrigate intracrevicularly to disrupt and dislodge the bio-lm, then thoroughly debride the implant surface with a curette. Irrigate a 2nd time to rinse out the debris and fur-ther detoxify the subgingival area. Pressure is then applied for one minute to obtain intimate soft tissue/restoration contact.• AlternativeAntiseptic;dilutedsodiumhypochlorite(NAOCl). - Diluted (.25%) NAOCl solution = one teaspoon (5ml) of standard 6% household bleach (Clorox) and diluting it with 4 oz (125ml) of water.• CheckOcclusion,possibleocclusalguard Treatment Regimen C: ANTIBIOTICS• Addsystemicand/orlocalantibiotictreatmentSystemic : Amoxicillin, Metronidazole (500 mg, 3 times/daily for 8 days)Alternative: Clindamycin, Augmentin, Tetracycline, Bactrim, CiprooxacinLocal : TetracyclineAlternative: , Doxycycline, Minocycline spheres (Arestin®)Treatment Regimen D: SURGERY (Access, Open Debridement, Bone Graft, Closure)Step 1: Access Flap, Open Debridement with Hand Instruments, Implantoplasty (Salvin Bur Kit)Step 2: Detoxify With:• 1.Apply0.12% or 0.2% Chlorhexidine with cotton pellet for 60 sec. (rinse with saline)+• 2a.Apply20-40% Citric Acid with cotton pellet or spatula or titanium brushes (Salvin) for 60 sec.(rinse with saline)OR• 2b.ApplyTetracycline Paste with titanium brushes (Salvin) for 60 sec. (rinse with saline) - Other Detoxication Agents: EDTA, Hydrogen Peroxide, 0.25% NAOCl - Er:YAG laser(diode laser alone results in an unacceptable increase in implant body temperature) Step 3: Bone Graft with Mineralized/Demineralized (70/30) + Autograft (if indicated)Step 4: Cross-Linked Collagen (Extended Collagen)Step 5: Tension-Free Closure with Vicryl (PGA) or PTFE sutures Treatment Regimen E: IMPLANT REMOVALLack of Keratinized TissuesLack of a zone of keratinized gingiva around teeth and oral implants is now recognized as serving an important clinical func-tion for implant health. Direct clinical evidence conrms the need for nonmobile keratinized tissue next to natural teeth. However, the tooth with the least amount of keratinized tissue is often the mandibular rst premolar.166 Yet this tooth is rarely the rst tooth lost from periodontal disease. If all other periodontal indices are normal, the amount or absence of keratinized gingiva has little to do with the expected longevity of the tooth. In longitudinal stud-ies, the lack of adequate keratinized and attached tissue does not compromise the long-term health of soft and hard tissue, as long as patients maintain good oral hygiene.167,168Many clinicians consider keratinized attached gingiva important to maintaining gingival health.169 Mucogingival considerations in restorative dentistry have been considered.170 ey concluded that if subgingival restorations were to be placed in areas of minimal keratin-ized gingiva with less than optimal plaque control, augmentation to widen the zone of keratinized tissue may be warranted.Although keratinized tissue around a tooth may not be manda-tory for long-term health, a number of benets are present with keratinized mucosa. e color, contour, and texture of the soft tis-sue drape should be similar around implants and teeth when in the esthetic zone. e interdental papillae should ideally ll the inter-proximal spaces. A high smile line often exposes the free gingival margin and interdental papillae zones. e keratinized tissue is more resistant to abrasion. As a result, hygiene aids are more comfortable to use, and mastication is less likely to cause discomfort.e degree of gingival recession appears related to the absence of keratinized gingiva. Root sensitivity and esthetic concerns may be associated with gingival recession. From a restorative dental aspect, keratinized mucosa is more manageable during the retrac-tion and impression-making process. Subgingival margin place-ment is improved, as is long-term stability in the presence of 1169CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesAB• Fig. . Ideal Keratinized Tissue. (A) Healthy tissue surrounding implant. (B) Preoperative evaluation measuring the amount of attached tissue.keratinized tissue. Many of these benets directly apply to the soft tissue around an implant.Natural teeth have two primary types of tissue: attached, kera-tinized gingiva and unattached, nonkeratinized mucosa. e type of tissue around a dental implant is more varied than natural teeth. After bone loss in the maxilla, excess tissue is often found, and the tissue is usually keratinized, unattached gingiva. An implant placed in the region may also have keratinized, unattached tissue. e tissues around the implant may also be similar to most natural teeth, surrounded by keratinized, attached gingiva (Fig. 41.16). e tissues may be nonkeratinized, unattached mucosa, more often in the mandible after bone height loss or after a bone graft and ap advancement to approximate the gingiva (Fig. 41.17). e nonkeratinized tissue may also be attached when acellular dermal matrix tissue (Oracell; Salvin Dental Specialities) is posi-tioned under the periosteum and bounds the overlying tissues to the bone. In theory, structural dierences in implants compared with teeth make them more susceptible to the development of inammation and bone loss when exposed to plaque accumula-tion or microbial invasion (e.g., less vascular supply, fewer bro-blasts, lack of connective tissue attachment, cementation).171Some reports indicate that the lack of keratinized tissue may contribute to implant failure. Kircsch et al. reported the most important criterion for implant health in the posterior man-dible was related to the absence or presence of keratinized gin-giva.172 In this report mobile, nonkeratinized mucosa exhibited greater probing depths, which was histologically conrmed. A study in monkeys found that an absence of keratinized mucosa increases the susceptibility of peri-implant regions to plaque-induced destruction.173e presence of keratinized tissue next to an implant presents some unique benets, compared with natural teeth. Keratinized gingiva has more hemidesmosomes; the junctional epithelial attachment zone may be of benet when in keratinized tissue. Whereas the orientation of collagen bers in the connective tis-sue zone of an implant may appear perpendicular to the implant surface, these bers in mobile nonkeratinized tissue run parallel to the surface of the implant.Mobile mucosa may disrupt the implant-epithelial attach-ment zone and contribute to an increased risk for inammation from plaque (Fig. 41.18).174 In addition to the general advantages of keratinized tissue stated for teeth, keratinized tissue around implants may also be benecial in several other ways. In a two-stage protocol the implant is less likely to become exposed dur-ing the healing process. e formation of an interdental/implant papillae is completely unpredictable with mobile nonkeratinized tissues. When the nonkeratinized tissue is mobile, several reports state that this is unsatisfactory.AB• Fig. . (A and B) Implants placed to retain a lower overdenture that are malpositioned with minimal attached tissue present. In these type of cases, the tissue will usually remain irritated, inflamed, and painful. 1170PART VIII Dental Implant MaintenanceA classication of attached gingiva and surgical alternatives to improve soft tissue types in edentulous sites for implant place-ment is critical for long-term implant survival.175 Ideal adequate keratinized tissue should be established clinically before implant placement, especially in the posterior regions.Interestingly, the studies that have advocated for the need for keratinized mucosa around dental implants have primarily inves-tigated implants with rough surfaces. Failure of rough-surface implants (e.g., hydroxyapatite-coated and plasma-sprayed cylinder-shaped implants) has been related to a lack of keratinized mucosa.176A meta-analysis reported 20% fewer instances of peri-implantitis in smooth-surface implants compared with rough-surface implants.177 Another benet of keratinized tissue is the clini-cal ease of treatment to reduce pocket depths if crestal bone loss occurs. Probing depths of 6 mm or more are more often associated with anaerobic bacteria. If the implant is out of the esthetic zone, a gingivectomy to reduce pocket depth is predictable. An apically positioned ap with nonkeratinized mucosa is less predictable and is more dicult to perform.e signicance of keratinized mucosa in the maintenance of dental implants with dierent surface conditions cannot be under-estimated. All 69 patients and 339 implants in the study had implant restorations for at least 3 years, and as long as 24 years, with an average of 8.1 years. Bleeding index, modied plaque index, gin-gival index, probing depth, width of attached keratinized mucosa, and amount of attached mucosa were recorded. In addition, average annual bone loss was calculated, using past and present radiographs. Gingival inammation and plaque accumulation were signicantly higher in patients with less than 2 mm of keratinized mucosa or 1 mm of attached mucosa. e surface condition of the implant was not statistically signicant in this study, although the smooth implants with less than 2 mm of keratinized mucosa were less stable than other groups relative to the soft tissue prole.In this study the average annual bone loss was not inuenced by the amount of keratinized or attached mucosa or the type of implant surface conguration (smooth versus rough). e great-est amount of bone loss was observed with rough implants in keratinized mucosa of less than 1 mm, but the dierence was not statistically signicant. e presence of keratinized mucosa was most signicantly advantageous in the soft tissue health of posterior implants, as indicated by the gingival index. Posterior implants, even in the presence of keratinized tissue, had a 3.5-fold higher annual bone loss than anterior implants in this study (0.14 versus 0.04 mm). Implant location appears to be more important than the presence or absence of keratinized mucosa.In most clinical situations attached keratinized gingiva is more desirable. A xed prosthesis (FP-1) in the esthetic zone requires keratinized mucosa to develop the soft tissue drape around the implant restorations. Mandibular overdentures also benet from a vestibule and zone of nonmobile keratinized tis-sue around the implant abutments to minimize the possibility of painful tissue.Management of Lack of Keratinized TissueSeveral surgical techniques to increase the amount of keratin-ized tissue around dental implants have been described in the literature: 1. Autogenous free gingival graft 2. Autogenous subepithelial connective tissue graft 3. Allogenic soft tissue grafts from human cadavers (e.g., Oracell; Salvin Dental) 4. Xenogenic soft tissue grafts from animalsAugmentation can be completed before surgery, concurrent with surgery, or after implant surgery. e most ideal time to graft is before surgery.Presurgical Augmentations 1. A trapezoidal ap is reected from the desired areas of grafting. 2. Full-thickness mucoperiosteal ap is the design of choice. 3. Autogenous or acellular dermal matrix (Oracell; Salvin Dental) is modied to the desired dimensions. 4. PGA or chromic suture is used (5–0 recommended) to secure allogenic dermal matrix (AlloDerm) to the recipient site. 5. Flap is modied to be tension free and pulled over to cover acellular dermal matrix and sutured with 4–0 or 5–0 with PGA or PTFE sutures (Fig. 41.19). Concurrent Augmentatione steps for concurrent augmentation are as follows: 1. e full-thickness ap is reected at the site of desired implant position (one tooth mesial and one tooth distal). 2. After implant placement and/or bone augmentation, autog-enous or acellular dermal matrix is layered over the augmen-tation site. 3. It is critical to have abundant tissue release (i.e., tension-free closure) to allow coverage of soft tissue over bone graft. 4. e ap is sutured with no tension and secured for primary intention healing with 4–0 or 5–0 with PGA or PTFE sutures (Figs. 41.20 and 41.21). AB• Fig. . (A and B) Maxillary implants with inadequate attached tissue. 1171CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesABCDE• Fig. . Free Gingival Graft. (A) Mandibular left first molar with compromised attached tissue. (B) Recipient site modified. (C) Palatal graft removed. (D) Palatal tissue graft. (E) Tissue graft sutured in place.AB• Fig. . Acellular Dermis. (A) Bone graft with inadequate attached tissue. (B) Acellular dermis placed around implant healing abutments. 1172PART VIII Dental Implant MaintenancePost-implant Tissue AugmentationAfter the soft tissue ap has healed, the soft tissue augmentation can be performed during the abutment change appointment or uncovery appointment (3 months of healing). e steps are as follows: 1. A full-thickness ap is reected, being wide enough to cover the size of the autogenous or acellular dermal matrix membrane. 2. Dermal matrix is ideally positioned and sutured to neighboring attached tissue (chromic 5–0). 3. e ap is advanced over the matrix, being careful to cover the entire allograft tissue (5–0 sutures are preferred). Retained Cement Peri-implant DiseaseCemented implant prostheses are used in implant dentistry because of the lower cost, relative simplicity, more passive t, improved esthetics, and similarity to traditional prosthetics. How-ever, with all of these advantages comes a signicant disadvantage, the retention of postoperative cement. e retained cement has been shown to harbor bacteria (similar to calculus with a natural tooth), which leads to peri-implant disease (Fig. 41.22).During implant restoration cementation, it is possible that excess cement can become extruded into the gingival sulcus around the implant. e presence of cement in the sulcus has been shown to cause complications such as discomfort, inamma-tion, soft tissue swelling, and bleeding or exudate on probing.178 It has been reported that cement can extrude at the implant abut-ment-interface when subgingival margins are present. Subgingi-val cement associated with an implant is more dicult to remove compared with a natural tooth, and various instruments used for this purpose have been shown to result in damage to implant abut-ments.179 It has been proposed that any mass of foreign material present adjacent to a dental implant has the potential to negatively impact health and survival of the implant. e specic material itself may determine how a disease process can manifest. Further, the use of cements intended for natural teeth may not be appro-priate for use with implant restorations.180Studies suggest that excess cement has been shown to be a possible cause of implant failure.181 Incidence of excess cement extrusion into peri-implant soft tissues and its adverse eects are well documented in the literature.182,183 Cement retains micro-bial ora similar to organisms responsible for inammatory periodontal diseases. e surface of retained cement has a rough topography, making removal of these microbes dicult, and can also result in accumulation signicant enough to form a peri-implant biolm similar to natural teeth.185,186 Clinical studies that have analyzed retained methacrylate-based cement samples from patients for bacterial colonization have shown a strong tendency for bacterial invasion by pathogens and opportunistic species.187 Remnant cement from implant restorations has been associated with consequences of increased bleeding on probing, suppura-tion, and peri-implant attachment loss.188 It is the formation of a peri-implant biolm that can cause the initiation and progres-sion of peri-implant mucositis and peri-implantitis diseases.189-191 Peri-Implantitis has been documented in several studies with a prevalence rate that ranges from 6% to as high as 47% of patients who have implants and have been followed over periods of 9 to 14 years.192-194e problem of excess cement has been associated with greater than 80% of cases of peri-implant disease. No particu-lar dierence or correlation could be associated with the type of cement used to lute the restoration in regard to either the presence of disease or treatment response (when comparing resin cement, resin-modied glass ionomer, zinc polycarboxylate, and glass ionomer). Further, the presence of cement retention and inammation was not dependent on the type of implant surface; titanium plasma–sprayed or sand-blasted large-grit acid-etched surfaces and titanium dioxide–blasted surfaces were ABC• Fig. . Acellular Dermis. (A) Five implants placed in the anterior mandible. (B) Dermis modified to fit over healing abutments. (C) Dermis placed over implants and healing abutments. 1173CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and Therapiescompared.195 In cases where cement is inadvertently left as an overhang or expressed into the peri-implant tissues, it should be detected and removed.Etiologye etiology of cement-retained peri-implantitis is as follows:Cement: e retained cement acts as a nidus for bacterial accu-mulation and proliferation. e roughened surface of the ce-ment inhibits the hygienic removal of the bacteria, which leads to peri-implant disease. Cement acts the same way as the etio-logic factor in periodontal disease.Sulcus-Teeth Versus Implant: Around natural teeth the junction-al epithelium and connective tissue attachment insert perpen-dicularly into the cementum, which tends to prevent the ow of excess cement into the sulcus. In contrast, the connective tis-sue around dental implants runs parallel, with no attachment into the implant surface. e ow of cement is not restricted, and it easily migrates apically (Fig. 41.23).Submucosal Margins: Margins of implant restorations are often placed more than 2 mm subgingivally for a better emergence prole and esthetics. However, studies have shown the deeper the margins, the more dicult the removal of cement. In mar-gins that are greater than 1.5 mm subgingivally, it is almost impossible to remove the cement totally.197Location: Retained cement may attach to the following: (1) crown, (2) abutment, and (3) bone. If the cement is pushed into the sulcular area and reaches the bone, signicant chronic issues will arise (Fig. 41.24).Timing: Perhaps one of the most interesting, yet troubling as-pects of cement-associated peri-implant disease is the range of time that can and has historically passed before obvious signs of an inammatory disease response is evident during clinical detection. Wilson and omas196 have shown that the time it takes for retained cement to become problematic and to eventually be diagnosed is in a range of 4 months to 9.3 years, with an average of 3 years. Another group showed detection ranging from several weeks to 4 years postcementa-tion. is documented that delayed detection in inamma-tory signs of peri-implant disease indicates a premise that ce-mented implant restorations should be examined periodically for disease.199 ABC• Fig. . Retained Cement. (A) Radiograph depicting retained subgingival cement. (B) Six months postoperatively. (C) Cement retention leading to failure of implant. 1174PART VIII Dental Implant MaintenanceRadiographic Evaluation: Several techniques are described in the literature to locate excess cement around implant restora-tions. ese include use of a dental endoscope and an invasive method of open ap debridement for direct observation.200,201 Radiographic examination has been shown to be eective at detecting excess cement overhangs in tooth-supported restora-tions and can serve as a less invasive method of detection for cement-retained implant-supported restorations.202,203 Radio-graphic examination is valuable in cement detection only if the luting agent has a high-enough radiodensity level.204It is signicant to note that with respect to restoration lut-ing cements and radiopacity, there is no currently established minimum radiopacity standard (however, there is currently a national standard radiopaque value mandated for all endodon-tic sealer cements; American National Standards Institute/ADA specication No. 57). erefore there is a broad range of radio-graphic visibility for restorative luting cements from having a highly radiopaque appearance to being completely undetect-able.205 Ideally, the luting agent should be more radiographi-cally dense than the titanium alloys. Cements that are zinc based (i.e., Fleck’s, Temp-Bond, Tempbond NE) have been shown to be most readily detectable radiographically with the higher gray level values. Studies have shown that many non-zinc-based cements are not detected radiographically, such as self-adhesive resin cement (RelyX Unicem), resin cement (Improv and Pre-mier Implant Cement), glass ionomer (RelyX), and calcium hydroxide (Dycal). Being able to evaluate the presence of excess cement and then determining whether removal is indicated is crucial to facilitate appropriate restorative protocols.206 After restoration cementation, residual excess cement has the high-est likelihood of detection at the interproximal aspects. It is at these sites where the accumulation of the bulk of excess cement produces the eect of an enhanced radiopacity described by one group as the “peripheral egg shell eect.”207 AB• Fig. . Different Attachment Systems for Implant Versus Tooth. (A) Circular fibers attach into the cementum, minimizing the possibility of cement retention. (B) Because an endosseous implant does not contain an attachment system with the tissue, retained cement can be easily extruded into the sulcular area. (From Resnik RR. Fixed prosthodontics complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complica-tions in Oral Implantology. St. Louis, MO: Elsevier; 2018; adapted from LeBeau J. Maintaining the long-term health of the dental implant and the implant-borne restoration. Compend Contin Educ Oral Hyg. 1997;3:3–10.)A B• Fig. . Cement Attachment Location. (A) Retained cement may adhere to the crown/abutment, peri-implant tissues, or the bone. (B) Implant with deep pathologic pocket associated with retained cement. 1175CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesType of cement: Many types of cement are used today in implant dentistry to retain implant-supported crowns. Agar et al.208 have shown that cement with resin components is the most dicult to remove from the abutment surface after cementa-tion. Cements containing zinc have been shown to be ideal for cementing implant crowns because they are the easiest to see radiographically. Zinc phosphate is a well-known popular cement choice, which makes retrievability dicult. In addi-tion, because of its solubility in the oral environment, a dry eld is denitely needed. Provisional cements are also popular in cementing implant crowns because they allow for retrieval. However, because provisional cements exhibit weaker reten-tive strengths, uncementation of the implant prosthesis may be problematic.Cememt ickness: ere is a large variation in the radiographic detection ability of cements. Some cements have a very high ra-diographic density, which allows for detection on radiographs. However, many cannot be detected, even at greater thickness (≈2 mm).Cementation technique: A common reason for retained cement is the cervical cementation technique, which usually parallels the technique for cementation on natural teeth. Most clinicians place an excessive amount of cement within the internal surface of the crown, which leads to extrusion in the sulcular area. PreventionSupragingival Margins. Excess retained cement may be mini-mized by designing the abutment margins supragingivally. How-ever, dentists are reluctant to place the margins at this level, especially if the crowns are in the esthetic zone. Studies have shown margins placed 1 mm supragingival or at the gingival mar-gins allow for ease of cement removal without a decreased chance of retention.209 Ideal Application of Cement. Controlling the amount of cement that is placed in the implant crown will allow for a decreased possibility of cement retention. Clinicians are reluctant to use a small amount of cement because this translates into the possibility of leakage and loss of retention.Excess cement may lead to improper seating, alteration of occlusion, and diculty in cement removal. Ideally a uniform thickness of 40 μm over the intaglio surface is ideal; however, in a clinical setting, this is very dicult. e internal surface of the crown may sometimes be irregular, and unequal ow patterns may exist between parallel and nonparallel surfaces.Additional factors that complicate ideal cementation are the cement’s ow properties, viscosity, dimensional stability, and wet-tability of the surfaces. Screw-Retained Prostheses. Although screw-retained implant prostheses have the disadvantages of higher cost and compro-mised esthetics in some cases, the lack of cement is a signicant advantage. Implant Abutment Modication. To reduce the amount of excess cement, studies have shown that modication of the abut-ment leads to less pressure and extruded cement. Ideally the abut-ment should be vented with two 0.75-mm radius vent holes, placed 3 mm apical to the occlusal area of the abutment and 180 degrees apart. is technique by Wadhwani et al.210 has been shown to limit the amount of cement extruded into the gingival sulcus of implant-retained crowns. TechniquesVarious techniques to reduce retained cement have been discussed in the literature. A popular technique is the abutment copy tech-nique, which uses Teon tape inside the intaglio surface before copying the abutment with a polyvinyl siloxane material. e cement-lled nal implant crown is seated on the copied abut-ment for excess cement removal before it is quickly transferred intraorally to be fully seated. is technique minimizes the pos-sibility of retained cement; however, it has limitations when cementing a multiple splinted implant prosthesis211 (Fig. 41.25).e Resnik technique (lubrication technique) uses water-sol-uble petroleum jelly placed on the outer surfaces of the crown or prosthesis and below the implant margin (i.e., sulcular area). A controlled cementation technique is utilized which controls the amount of cement used and also allows for the removal of excess cement prior to nal cementation. e advantage of this tech-nique allows for the prevention of cement from adhering to the crown, sulcus, or underlying bone (Box 41.5 and Fig. 41.26). Removal of Retained Implant CementEven the most diligent and skilled implant clinician may leave resid-ual cement in the sulcular area of implant crowns. e importance of postoperative appointments for implant patients after cementa-tion of the restoration cannot be overemphasized. Regular main-tenance is extremely crucial for cement-retained crowns. Possible symptoms that may warrant an evaluation for retained cement are localized inammation, bleeding on probing, exudate, progressively increased probing depths, and radiographic bone loss.NonsurgicalNonsurgical treatment includes regular curettage with hand instruments. It should be noted it is very dicult to remove all cement non-surgically. SurgicalIn many cases, surgical access is necessary for complete cement removal, which includes ap, curettage, and detoxication with possible grafting. In cases of peri-implant disease the detection and removal of excess cement have frequently (76% of aicted patients) resulted in resolution of clinical inammatory signs in as little as a month posttreatment. is was possibly due to removal of cement irritants causing both bacterial and mechanical insult. Some authors advocate hand scalers, piezoelectric, and magnetostrictive mechani-cal devices (along with the benet of a dental endoscope instrument for direct visualization of cement deposits)212 (Fig. 41.27). Peri-implant Mucosal Hyperplasiae gingival overgrowth results in extreme diculty for the patient to maintain adequate hygiene and for the clinician in performing debridement. When gingival overgrowth is asso-ciated with radiographic bone loss, the resultant periodontal pockets are expressed as “true” periodontal pockets. If there is no associated bone loss, the pockets are termed “pseudo” pockets or gingival pockets.213Gingival hyperplasia may also result in an esthetic issue for the patient. is will require surgical intervention to reduce the tis-sue. In addition, gingival hyperplasia may make it impossible for a prosthesis to be completely seated (i.e., bar overdenture) or give rise to chronic tissue soreness. 1176PART VIII Dental Implant MaintenanceStep 1:Applywater-solublepetroleumjellytotheoutermarginofthecrownwitha1-mLtuberculinsyringe.Step 2:Sealtheabutmentscrew(cottonball,Teontape)withoutsealingtheentireaccess.Step 3:Placeathinlayerofpetroleumjelly360degreeswitha1mLtuberculinsyringewithinthesulcusandaroundtheimplant.Step 4:Applyathinlayer(≈40μm)ofcementtotheintagliosurfaceofthecrownabutment.Step 5:Seatcrown,removecrown,removeexcesscementadheredtotheoutermarginsurface,andremoveanysulcularexcesscementandpetroelumjellywithabrush.Step 6:Reseatcrown,evaluateforanyexcesscement. • BOX 41.5 Cementation Technique (Resnik Technique)ABCDEF• Fig. . Cementation Technique. (A) Polytetrafluoroethylene tape placed over abutment. (B) Crown inserted onto abutment. (C) Polyvinyl impression material added to the internal surface of the crown to make an abutment duplicate. (D) Internal surface of crown: abutment inserted onto implant in the mouth. (E) Cement added to crown and placed on polyvinyl abutment duplicate. (F) Excess cement removed, then inserted onto abutment in mouth. 1177CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesA BCDEFG• Fig. . Alternative Cementation Technique. (A) Outside of the crown is lubricated with water-sol-uble petroleum jelly. (B) Illustration-Water-soluble jelly placed within the sulcus with a 1-mL tuberculin syringe. (C) Clinical image after sulcular lubricant placed, (D) Cement is placed into the internal surface of the crown. (E) Crown is inserted into mouth. (F) Crown is removed and excess cement is removed with a brush. (G) Crown is reinserted onto abutment. 1178PART VIII Dental Implant MaintenanceABCDEF• Fig. . Retained Cement. (A) Implant restoration in function for 6 months with persistent signs of peri-implant mucositis. (B) Radiographically evident manifestation of remnant cement at the restorative margin. (C) Excess cement after instrumentation with titanium and plastic curettes. (D) Peri-implant tissues immediately after instrumentation. (E) Radiograph demonstrating excess cement has been removed. (F) Condition of peri-implant tissues at 6-week reevaluation appointment. 1179CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesEtiologyAfter clinical diagnosis of implant-related gingival overgrowth, potential etiologies must be identied, such as hormonal, medica-tion induced, allergy induced, or patient-related habits. Various hormonal factors (e.g., related to pregnancy or puberty) and med-ications have been associated with the gingival overgrowth. Medi-cations such as phenytoin (i.e., Dilantin), immunosuppressants (e.g., cyclosporine), calcium channel blockers, and amphetamines have been associated with gingival hyperplasia.Gingival overgrowth has also been associated with patient hab-its such as mouth breathing. Allergy-induced hyperplasia is also becoming more prevalent in implant dentistry. With the use of titanium alloys for the fabrication of the dental implants and abut-ments, exacerbated allergic reactions are becoming a more common problem. Nickel (Ni), combined with titanium or in the nal pros-thesis, may exacerbate and cause an acute allergic reaction. Alumi-num (Al) and beryllium (Be) have been associated with eczema and soft tissue reactions that result in gingival overgrowth. PreventionIf a patient is considered to be at high risk for implant-related gin-gival hyperplasia (e.g., because of medications), he or she should be instructed to maintain meticulous oral hygiene. In addition, a more frequent recall protocol (four times per year) should be implemented that includes debridement. e prosthesis should be evaluated and maintained with a minimum of 1 mm of space between the tissue and the prosthesis, for ease of cleaning and prevention of prosthesis-induced irritation. Managemente treatment of peri-implant hyperplasia should begin with conven-tional periodontal therapies to reduce plaque biolm and inamma-tion. e surgical management of implant gingival overgrowth may require gingivectomy (if adequate keratinized gingiva is present) or apically positioned aps (without adequate keratinized gingiva).e use of 0.12% or 0.2% chlorhexidine twice per day has been shown to be successful in reducing tissue overgrowth and bacteria counts. When gingival hyperplasia is present around implants associated with overdentures, care should be exercised to minimize further enlargement (Fig. 41.28).Commonly, practitioners will relieve the denture so the path of insertion does not cause irritation or mucosal injury. is may lead to inadequate thickness of acrylic, predisposing the prosthe-sis to fracture. Ideally the tissue enlargement should be reduced and the causative agent identied and treated accordingly. It is important to note that even with meticulous care and removal of etiology, gingival overgrowth may recur. Communication with the patient is key to avoid misunderstanding (Box 41.6). Implant Quality Scalee criteria for success in implant dentistry remain complex. Most clinical studies reporting success and failure do not qualify the type of success achieved. Instead, the term success primarily has been used interchangeably with survival of the implant. e term failure has been used to indicate the implant is no longer present in the mouth. Nearly all reports in the prosthetic literature also report survival as success.What is success for a natural tooth? In the periodontal literature a quality of health is presented, and well-established guidelines based on clinical criteria describe the ideal health of natural teeth. e general term success in implant dentistry should be replaced with the concept of quality of health, with a health-disease con-tinuum describing the status of implants.AB• Fig. . Hyperplasia. (A and B) Hyperplastic tissue growth surround-ing existing implant prosthesis resulting in home care difficulty. (From Suzuki JB, Misch CE. Periodontal and maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implan-tology. St. Louis, MO: Elsevier; 2018.)AnticonvulsantsPhenytoinPhenobarbitalLamotrigineVigabatrinEthosuximideTopiramatePrimidoneCalcium channel blockersNifedipineAmlodipineVerapamilImmunosuppressant drugsCyclosporineSystemic factorsPregnancyPubertyVitaminCdeciencyLeukemiaNeoplasms(bromas,papillomas,carcinomas) • BOX 41.6 Pharmacologic Agents That Cause Gingival Hyperplasia 1180PART VIII Dental Implant Maintenance Implant Quality ScaleImplant Quality Scales Clinical Conditions Suzuki-Resnik ProtocolSuccess (optimal health)Osseointegration/Stage0osseoseparationNopainortendernessuponfunction0mobility<2mmradiographicbonelossfrominitialsurgeryPD<4mmNosuppurationNoBOPProtocol1Survival (satisfactory health)StageIosseoseparationPeri-mucositisNopain0mobility<2mmradiographicbonelossfrominitialsurgeryPeri-mucosalinammationPD±4mm(bleedingand/orsuppurationonprobing)Protocol2Survival (potentially compromised)StageIIosseoseparationEarlyperi-implantitisNopain0mobility2–4mmradiographicbonelossPD±4mm(bleedingand/orsuppurationonprobing)Peri-mucosalinammationBoneloss<25%oftheimplantlengthProtocol2orProtocol3Survival (compromised health)StageIIIosseoseparationModerateperi-implantitisVariablepain0mobilityPeri-mucosalinammationPD≥6mm(bleedingand/orsuppurationonprobing)Boneloss25%–50%oftheimplantlengthProtocol3Failure (clinical failure)StageIVosseoseparationAdvancedperi-implantitisPeri-mucosalinammationPainuponfunctionPD>8mm(bleedingand/orsuppurationonprobing)Boneloss>50%oftheimplantlengthMobilityUncontrolledexudateMaybenolongerinmouthProtocol4Others(suchasretrograde peri-implantitis)Variableperi-mucosalinammationRadiographically:periapicallesionaroundimplantClinical:pain,tenderness,stulaformationorswellingSurgicalreentryandrevisionorremovalofimplantBOP, bleeding on probing; PD, probing depth; SPT, supportive periodontal therapy.From Suzuki JB, Misch CE. Periodontal and maintenance complications. In: Resnik RR, Misch CE, eds. Misch’s Avoiding Complications in Oral Implantology. St. Louis, MO: Elsevier; 2018. Data from Suzuki JB, Hsiao YJ, Misch CE. Personal communication, 2017. TABLE 41.4Success criteria for endosteal implants have been proposed pre-viously.214-218 e Misch scale proposes management modalities corresponding to dierent treatment levels.219e most recent Suzuki-Misch-Hsiao implant health scale was published in Resnik and Misch’s Avoiding Implant Complications (2017).220 e Suzuki-Misch-Hsaio scale presented implant qual-ity of health based on clinical evaluation (Table 41.4). is quality of health scale allows the implant dentist to evaluate an implant using the listed criteria, place it in the appropriate category, and then treat the implant accordingly. e prognosis also is related to the quality scale.Ideal clinical conditions for natural teeth include absence of pain, less than 0.1 mm of initial horizontal mobility under lateral forces of less than 100 g, less than 0.15 mm of secondary mobility with lateral forces of 500 g, absence of observed vertical mobil-ity, periodontal probing depths of less than 2.5 mm, radiographic crestal bone height 1.5 to 2.0 mm below the cementoenamel junction, intact lamina dura, no bleeding on probing, no exudate, and absence of recession or furcation involvement on multirooted teeth.e American Dental Association CDT (2018) has dened ve periodontal types for diagnosis and treatment of natural teeth.221,222 e American Dental Association’s categories of disease do not simply indicate success or failure but rather a range from health to disease. is classication allows a clini-cal approach to treatment in each category. A similar scale for implants has been established as an aid to diagnosis and treat-ment that also proposes management approaches according to the signs and symptoms.Group I: Optimum HealthGroup I represents implant success with optimum health condi-tions. No pain is observed with palpation, percussion, or func-tion. No mobility is noted in any direction with loads less than 500 g of implant movement (IM). Less than 2.0 mm of crestal 1181CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesAB• Fig. . Group I: Optimum Health. (A and B) Ideal implants with no associated bone loss.bone has been lost since the placement of the implant. is bone loss is typically a result of the implant biologic width below the abutment connection and surface of the implant. e implant has no history of exudate, and no radiolucency is present around the implant body. e probing depth is equal to or less than 5 mm and is stable after the rst year. Ideally the bleeding index is 0 to 1. Group I implants follow a normal maintenance program every 6 months. e prognosis is very good to excellent (Fig. 41.29). Group II: Satisfactory HealthGroup II implants exhibit satisfactory health and are stable. No tenderness is observed on palpation, percussion, or func-tion. No observable implant mobility was present in the hori-zontal or vertical direction with loads less than 500 g. Crestal radiographic bone loss is observed between 2 and 4 mm from implant placement. e most common cause is the early load-ing bone loss related to the amount of occlusal force and the density of the bone. No pain is observed. Probing depths may be as much as 5 to 6 mm because of the original tissue thickness and marginal bone loss, but are stable. Bleeding on probing index is often 1 or even 2. ese implants may be con-sidered to have peri-implant mucositis. e treatment indicated for group II implants consists of a stress reduction protocol for the implant system, shorter intervals between hygiene appoint-ments (e.g., 3 months), reinforcement of oral hygiene instruc-tions, annual radiographs until the crestal bone has stabilized, and gingivoplasty or sulcus reduction procedures where indi-cated. e prognosis is good to very good depending on the depth of the implant sulcus.For pockets less than 6 mm in depth, the following can be concluded: 1. Mechanical therapy alone or combined with chlorhexidine results in the clinical resolution of peri-implant mucositis lesions. 2. Histologically both treatments result in minimal inammation compatible with health. 3. e mechanical eect alone is sucient to attain clinical and histologic resolution of mucositis lesions (Fig. 41.30). A B• Fig. . Group II: Satisfactory Health. (A and B) Implants exhibit satisfactory health and are stable, but tenderness is observed on palpation, percussion, or function. 1182PART VIII Dental Implant MaintenanceAB• Fig. . Group III: Compromised Survival. (A and B) Implants are classified as compromised survival and exhibit a slight-to-moderate peri-implantitis and compromised health status.Group III: Compromised SurvivalGroup III implants are classied as compromised survival and exhibit a slight-to-moderate peri-implantitis and compromised health status. Peri-implantitis is dened as an inammatory process aecting the tissue around an implant that results in loss of supporting bone.Group III implants are characterized by radiographically evi-dent vertical bone loss, peri-implant pocket, bleeding on probing (plus occasional suppuration), and mucosal swelling and redness but no pain on function.ese implants warrant more aggressive clinical therapy. No pain is apparent in function, but tenderness may be slight on percussion or function. No vertical or initial horizontal mobil-ity (IM-0) is evident. Greater than 4 mm of crestal bone loss has occurred since implant insertion but less than half the length of the implant. Greater than 7 mm and increasing probing depths are also present, usually accompanied by bleeding when probing. Exudate episodes may have lasted more than 1 to 2 weeks and may be accompanied by a slight radiolucency evident around a crestal region of the implant.Group III implants warrant aggressive surgical and prosthetic intervention. Stress factors are also addressed. e prosthesis may be removed in nonesthetic regions. If a bar (used to support and retain an overdenture) is present, it may be removed during the surgical therapy. Modication of the occlusal scheme and meth-ods to decrease the forces in the aicted regions after hard and soft tissue surgical treatment include decreasing cantilever length, occlusal adjustment, and occlusal splint therapy.In cases of rapid bone changes, the prosthesis design may be modied completely from a xed to a removable restoration to stress relief and soft tissue support. Additional implants to support the restoration may be indicated, especially if the patient is unwill-ing to wear a removable prosthesis.Systemic and topical antibiotics and local chemical agents such as chlorhexidine are indicated in the presence of exudate. However, this method is usually of short-term benet if the causative agents of implant failure are not eliminated.Surgical management most often consists of soft tissue removal or exposure of a portion of the implant. Bone grafts may be used together with these approaches around the implant. A three-step approach is implemented for this category in the following order: (1) antimicrobial therapy (local or systemic), (2) stress reduction, and (3) surgical intervention.e prognosis is good to guarded, depending on the ability to reduce and control stress after the surgical corrections have improved the soft and hard tissue health (Fig. 41.31). Group IV: Clinical FailureGroup IV of implant health is clinical or absolute failure. e implant should be removed under any of these conditions: (1) pain on palpation, percussion, or function; (2) greater than 0.5 mm of horizontal mobility; (3) any vertical mobility; (4) uncon-trolled progressive bone loss; (5) uncontrolled exudate; (6) more than 50% bone loss around the implant; (7) generalized radiolu-cency; or (8) implants surgically placed but unable to be restored (sleepers). Implants that are surgically removed or exfoliated are also in the category of failure.is category also includes implants surgically removed or exfoliated and no longer in the mouth. e remaining edentu-lous area often is treated with autogenous, synthetic, or other substitute bone graft materials to replace the missing bone. After the favorable bony conditions are augmented, implants may be inserted again with a good prognosis.e terminology for implant failure often is confusing, with dierent terms describing similar situations. Terminology for implant failure using the time period of failure has been suggested as a primary criterion. Many implant failures are not described ideally by the time of the complication and are not addressed in this nomenclature. 1183CHAPTER 41 Peri-Mucositis and Peri-Implantitis Diagnosis, Classication, Etiologies, and TherapiesABC• Fig. . Group IV: Implant Failure. (A–C) Implants are deemed absolute failures.Occasionally the patient will not permit removal of the implant. Regardless of whether the patient returns for implant removal, the implant is recorded as a failure in all statistical data. e patient should be warned against the irreversible damage to the surround-ing bone with implants retained in this condition. Consideration should be given to their removal because future treatment may be compromised (Fig. 41.32). ConclusionOnce the surgical and prosthetic phases of implant therapy have been completed, the work of the clinician is not over. Patients must be educated regarding proper maintenance of their implant-supported restorations, and routine examinations should be performed to monitor overall health. Many dierences exist in the biology of natural teeth compared with implant-supported restorations as they pertain to periodontal status. It is critically important that the implant clinician recognize these dierences, properly diagnose disease states, and eectively manage these problems should they arise. By understanding the etiologies of the various peri-implant disease states, a clinician can work with the patient to build an eective protocol of prevention (Figs. 41.33 and 41.34). 1184PART VIII Dental Implant MaintenanceAB CDEF GHI• Fig. . Peri-implant Disease Protocol. (A) Maxillary right central incisor implant with associated bone loss and poor tissue health. (B) Radiographic evidence of peri-implant disease. (C) Tissue reflection revealing osseous defect. (D) Implantoplasty (removal of surface threads) and detoxification. (E) Bone grafting and collagen membrane placed. (F) Subepithelial connective tissue graft. (G) Final closure. (H) Immediate postoperative radiograph. (I) One-year follow-up. A BCDEF• Fig. . Peri-implant Disease Protocol. (A) Mandibular left first molar bone loss. 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