19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.16-0488 by Readcube (Labtiva Inc.), Wiley Online Library on [22/01/2023].

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Received: 25 July 2016 Revised: 1 August 2017 Accepted: 8 September 2017
DOI: 10.1002/JPER.16-0488

2017 WORLD WORK SHOP

Peri-implant mucositis

Lisa J.A. Heitz-Mayfield1,2 Giovanni E. Salvi3

1 Department of Anatomy, Biology and

Human Physiology, International Research Abstract

Collaborative-Oral Health and Equity, Univer-
Objectives: This narrative review was prepared for the 2017 World Workshop of the
sity of Western Australia, IRCOHE, Crawley,
WA, Australia American Academy of Periodontology and European Federation of Periodontology
2 Faculty of Dentistry, University of Sydney, to address key questions related to the clinical condition of peri-implant mucositis,
Surry Hills, NSW, Australia including: 1) the definition of peri-implant mucositis, 2) conversion of peri-implant
3 Department of Periodontology, University of
health to the biofilm-induced peri-implant mucositis lesion, 3) reversibility of peri-
Bern, Bern, Switzerland
implant mucositis, 4) the long-standing peri-implant mucositis lesion, 5) similarities
Correspondence
Dr. Lisa JA Heitz-Mayfield, 4 McCourt St, and differences between peri-implant mucositis at implants and gingivitis at teeth, and
West Leederville, WA 6007-6009. 6) risk indicators/factors for peri-implant mucositis.
Email: heitz.mayfield@iinet.net.au
The proceedings of the workshop were Methods: A literature search of MEDLINE (PubMed) and The Cochrane Library
jointly and simultaneously published in the up to and including July 31, 2016, was carried out using the search strategy (peri-
Journal of Periodontology and Journal of
implant[All Fields] AND (“mucositis”[MeSH Terms] OR “mucositis”[All Fields]))
Clinical Periodontology.
OR (periimplant[All Fields] AND mucosits[All Fields]). Prospective, retrospective,
and cross-sectional studies and review papers that focused on risk factors/indicators
for peri-implant mucositis as well as experimental peri-implant mucositis studies in
animals and humans were included.

Findings: Peri-implant mucositis is an inflammatory lesion of the soft tissues sur-

rounding an endosseous implant in the absence of loss of supporting bone or con-
tinuing marginal bone loss. A cause-and-effect relationship between experimental
accumulation of bacterial biofilms around titanium dental implants and the devel-
opment of an inflammatory response has been demonstrated. The experimental peri-
implant mucositis lesion is characterized by an inflammatory cell infiltrate present
within the connective tissue lateral to the barrier epithelium. In long-standing peri-
implant mucositis, the inflammatory cell infiltrate is larger in size than in the early
(3-week) experimental peri-implant mucositis lesion. Biofilm-induced peri-implant
mucositis is reversible at the host biomarker level once biofilm control is reinstituted.
Reversal of the clinical signs of inflammation may take longer than 3 weeks. Factors
identified as risk indicators for peri-implant mucositis include biofilm accumulation,
smoking, and radiation. Further evidence is required for potential risk factors, includ-
ing diabetes, lack of keratinized mucosa, and presence of excess luting cement.

© 2018 American Academy of Periodontology and European Federation of Periodontology

J Periodontol. 2018;89(Suppl 1):S257–S266. wileyonlinelibrary.com/journal/jper S257

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S258 HEITZ-MAYFIELD AND SALVI

Conclusions: Peri-implant mucositis is caused by biofilm accumulation which dis-

rupts the host–microbe homeostasis at the implant–mucosa interface, resulting in
an inflammatory lesion. Peri-implant mucositis is a reversible condition at the host
biomarker level. Therefore, the clinical implication is that optimal biofilm removal
is a prerequisite for the prevention and management of peri-implant mucositis. An
understanding of peri-implant mucositis is important because it is considered a pre-
cursor for peri-implantitis.

KEYWORDS
peri-implant disease, peri-implant mucositis, peri-implantitis, risk factor, risk indicator

Peri-implant diseases, including peri-implant mucositis and implant bone.1–3 The important criteria for the definition of
peri-implantitis, were first defined and described at the peri-implant mucositis are inflammation in the peri-implant
First European Workshop on Periodontology in Ittingen in mucosa and the absence of continuing marginal peri-implant
1993.1 Following this, there have been numerous workshops bone loss. The clinical sign of inflammation is bleeding
addressing the definition, prevalence, and treatment of these on probing, while additional signs may include erythema,
diseases.2,3 Peri-implant mucositis is considered to be the swelling, and suppuration (Table 1). The clinical case defini-
precursor of peri-implantitis. The objective of this narrative tion of peri-implant mucositis has been addressed in another
review was to address key questions related to peri-implant review prepared for this workshop.
mucositis, including: 1) the definition of peri-implant mucosi-
tis, 2) conversion of peri-implant health to the biofilm-induced
peri-implant mucositis lesion, 3) reversibility of peri-implant
mucosits, 4) the long-standing peri-implant mucositis lesion,
CONVERS IO N FROM HEALTH Y
5) similarities and differences between peri-implant mucosi-
PERI-IMPLANT MUCOSA TO
tis at implants and gingivitis at teeth, and 6) risk indica-
PERI-IMPLANT MUCOSITIS
tors/factors for peri-implant mucositis.
Healthy peri-implant mucosa is characterized by the presence
of an oral epithelium extending into a non-keratinized bar-
M AT E R I A L S A N D M E T H O D S rier epithelium with basal lamina and hemidesmosomes fac-
ing the implant or abutment surface.4 In the connective tissue
A literature search of MEDLINE (PubMed) and The adjacent to the epithelial barrier, inflammatory cell infiltrates
Cochrane Library up to and including July 31, 2016, was representing the host's defense against the bacterial challenge
carried out using the search strategy (peri-implant[All Fields] are present. In healthy peri-implant mucosal conditions, the
AND (“mucositis”[MeSH Terms] OR “mucositis”[All barrier epithelium and the presence of scattered inflammatory
Fields])) OR (periimplant[All Fields] AND mucositis[All cells constitute the soft tissue seal separating the peri-implant
Fields]), resulting in 224 papers. Prospective, retrospective, attachment from the oral cavity.5–9
and cross-sectional studies and review papers focused on Peri-implant mucositis develops from healthy peri-implant
risk factors/indicators for peri-implant mucositis as well as mucosa following accumulation of bacterial biofilms around
experimental peri-implant mucositis studies in animals and osseointegrated dental implants. A cause-and-effect relation-
humans were included. Following discussion, the current ship between experimental accumulation of bacterial biofilms
authors agreed on the studies to be included in this narrative around titanium dental implants and the development of
review based on their relevance to the questions, outlined an inflammatory response (i.e., experimental peri-implant
above, addressing the topic of peri-implant mucositis. mucositis) has been demonstrated in humans.10–13
In an early study by Pontoriero et al.,10 twenty partially
D EFINITION OF PE R I - I MP L A N T edentulous patients received dental implants following suc-
M U CO S I T I S cessful completion of periodontal therapy. After 6 months of
supervised oral hygiene, the peri-implant mucosa was charac-
Peri-implant mucositis has been defined in previous work- terized by the absence of obvious signs of clinical inflamma-
shops as an inflammatory lesion of the mucosa surround- tion. Following this period, the patients were asked to abolish
ing an endosseous implant without loss of supporting peri- oral hygiene practices for 3 weeks. At the end of this period,
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.16-0488 by Readcube (Labtiva Inc.), Wiley Online Library on [22/01/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
HEITZ-MAYFIELD AND SALVI S259

TABLE 1 Similarities and differences between biofilm-induced gingivitis and peri-implant mucositis
Gingivitis Peri-implant mucositis
Definition Gingival inflammation without periodontal Peri-implant mucosal inflammation in absence of
attachment loss continuous marginal peri-implant bone loss
Clinical signs Redness, swelling, and bleeding on gentle Redness, swelling, bleeding on gentle probing, and
probing suppuration
Experimental inflammation Increase in bleeding sites during experimental Experimental peri-implant mucositis leads to greater
in humans gingivitis12,13 increase in bleeding sites compared with
experimental gingivitis.12,13
Reversibility in humans Experimental gingivitis clinically reversible after Experimental peri-implant mucositis may take
reinstitution of biofilm control14 longer than 3 weeks for clinical reversibility.12,13
Resolution of host biomarkers in gingival Resolution of host biomarkers in peri-implant
crevicular fluid following 21 days of crevicular fluid following 21 days of reinstituted
reinstituted biofilm control12,13 biofilm control12,13

Analysis of human biopsies Experimental biofilm accumulation results in Increased proportions of inflammatory cells in
increased proportions of inflammatory cells in connective tissue similar to those found in
connective tissue11 experimental gingivitis11
Short- vs. long-standing 3-week and 3-month experimental biofilm 3-month experimental biofilm accumulation in dogs
inflammation accumulation results in similar intensity of results in a more pronounced inflammatory
inflammatory responses in gingiva of dogs17,72 response in peri-implant mucosa compared with
inflammatory response in the gingiva17
Inflammatory lesions from long-standing mucositis
in humans20 considerably larger compared with
those of short-term (3-week) experimental
mucositis lesions11

Variability in humans High and low responders to experimental biofilm High and low responders to experimental biofilm
accumulation73 accumulation not yet identified

optimal biofilm control was reinstituted. At all examinations Outcomes of a comparative study in humans by Salvi
the following clinical parameters were assessed around the et al.12 indicated that 3 weeks of experimental biofilm accu-
implants: plaque index (PI), gingival index (GI), sulcus bleed- mulation resulted in a higher proportion of bleeding sites in
ing index (SBI), probing depths (PD), and marginal recession the peri-implant mucosa when compared with that in the gin-
(REC). The 3-week period of abolished oral hygiene prac- giva. In that study, the PI at tooth sites was significantly ele-
tices revealed the development of visible signs of mucosal vated when compared with that at implant sites after 3 weeks
inflammation, such as swelling, redness, and bleeding. This of abolished oral hygiene.12 However, the increase of the GI
cause-and-effect relationship between the accumulation at tooth sites was significantly lower compared with that at
of bacterial biofilms and the development of peri-implant implant sites, indicating that a comparable bacterial challenge
mucositis is consistent with the results obtained in the exper- yielded a more severe inflammatory response at implant sites.
imental gingivitis model by Löe et al.14 In another study by A recent study, by Meyer et al.,13 compared clinical and
Zitzmann et al.11 involving 12 partially edentulous patients biologic responses during experimental gingivitis and peri-
the inflammatory. The inflammatory response to the experi- implant mucositis in subjects aged ≥70 years. Although less
mental bacterial challenge was characterized by the enumer- biofilm accumulation was observed at implant sites, the peri-
ation of the proportions of T- and B-cells in peri-implant implant mucosa yielded a higher proportion of bleeding sites
tissues. Biopsies harvested around implants in a clinically compared with that observed in the gingiva,13 thus confirm-
healthy situation and after 21 days of experimental biofilm ing the results by Salvi et al.12 obtained in a younger patient
accumulation indicated that the connective tissue surround- sample.
ing the implants displayed an increased volume of T- and
B-lymphocytes as a consequence of abolished oral hygiene IS BIOFILM-INDUCED
practices.11 It was also noted that the size of the inflamma- PERI-IMPLANT MUCOSITIS
tory cell infiltrate and the number of several immune cell A REVERSIBLE DISEASE?
populations was not significantly different when comparing
biopsies from gingiva at teeth and biopsies from peri-implant Although a cause–effect relationship between experimental
mucosa.11 biofilm accumulation and the development of experimental
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.16-0488 by Readcube (Labtiva Inc.), Wiley Online Library on [22/01/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
S260 HEITZ-MAYFIELD AND SALVI

peri-implant mucositis was claimed in the two studies men- biofilm accumulation.16,17 In these dog studies, comparisons
tioned previously,10,11 the case for a true cause–effect rela- were made between the response of the gingiva at teeth and
tionship would be strengthened by the proof of reversibility the peri-implant mucosa at implants. Clinical examinations,
to pre-experimental levels of mucosal health. In the study by biofilm sampling, and biopsies were obtained at both the early
Salvi et al.,12 the GI at implant sites dropped significantly less and long-standing inflammatory lesions. At 3 weeks there was
compared with that at tooth sites following 3 weeks of rein- abundant biofilm accumulation, and both the gingiva and the
stituted oral hygiene practices. Moreover, pre-experimental peri-implant mucosa showed clinical signs of inflammation.
levels of GI were not reached at implant sites 21 days after Histology showed an inflammatory cell infiltrate within the
reinstitution of self-performed biofilm control.12 This indi- connective tissue which was found in the marginal portion of
cated that resolution of experimental peri-implant mucositis the soft tissues, immediately adjacent to the barrier epithelium
in humans may take longer than 3 weeks (Table 1). In contrast at implants and the junctional epithelium at teeth.16 In con-
to the study by Salvi et al.,12 all clinical parameters assessed trast, after a longer period (90 days) of undisturbed biofilm
in an elderly patient sample (i.e., ≥70 years) returned to pre- accumulation, the peri-implant mucositis lesions contained
experimental levels after 3 weeks of reinstituted biofilm con- a smaller number of fibroblasts than the gingival counter-
trol, thus documenting reversibility of experimentally induced parts, and the area occupied by the inflammatory infiltrate
peri-implant mucositis.13 was greater in the peri-implant mucositis lesions than the gin-
Resolution of experimental peri-implant mucositis was givitis lesions, although it did not extend beyond the barrier
achieved in both studies at the host biomarker level, as identi- epithelium.17
fied by the decrease to pre-experimental values of crevicular Ericsson et al.,18 in an experimental dog study, obtained
fluid pro-inflammatory biomarkers.12,13 These outcomes12,13 biopsies of peri-implant mucosa after 9 months of biofilm
corroborated the findings of a study in which levels of inter- accumulation and showed an inflammatory infiltrate located
leukin (IL)-1𝛽, tumor necrosis factor-alpha (TNF-𝛼), and within the marginal portion of the peri-implant mucosa. In
transforming growth factor-beta2 (TGF-𝛽2) were determined another experimental study in the dog model, long-standing
in crevicular fluid samples of 25 subjects before and after a biofilm-associated lesions of 5 months duration were estab-
3-week period of abolished oral hygiene and after 69 days lished in the peri-implant mucosa adjacent to three different
of re-established oral hygiene practices.15 While TNF-𝛼 and implant systems.19 The findings of this study confirmed that
TGF-𝛽2 levels did not change during the experimental period, the size and apical extension of the inflammatory infiltrate did
IL-1𝛽 yielded a significant increase after 3 weeks of abolished not extend beyond the barrier epithelium for all three implant
oral hygiene and was reversed to pre-experimental levels after systems used.
69 days.15 Although the period of reinstituted oral hygiene
was shorter at 3 weeks in the studies by Salvi et al.12 and
Meyer et al.,13 IL-1𝛽 crevicular fluid levels returned to pre- Human studies
experimental values, thus confirming the outcomes obtained Experimental studies in humans have evaluated the response
by Schierano et al.15 to 3 weeks of biofilm accumulation, corresponding to the
time frame of the experimental gingivitis study by Löe
et al.,14 where reversibility of the inflammatory lesion around
EXPERIMEN TA L P E R I - I MP L A NT
teeth was demonstrated after reinstitution of biofilm con-
M U CO S I T I S M O D E L S V E R S U S
trol after 3 weeks. There are studies reporting on human
LONG-STANDING PERI-IMPLANT
biopsies of peri-implant tissues where long-standing peri-
M U CO S I T I S L E S I O N S
implant mucositis lesions were evaluated.20,21 Gualini et al.20
described the immunohistochemical features of peri-implant
Experimental studies in humans and animals have demon-
mucositis lesions obtained from 10 partially edentulous sub-
strated that de novo biofilm accumulation results in an inflam-
jects with implants in function between 2 and 5 years. Clin-
matory lesion within the peri-implant mucosa with migration
ically, the degree of redness and swelling of the inflamed
of leukocytes through the barrier epithelium and the establish-
tissues varied; however, all sites bled on gentle probing.
ment of an inflammatory infiltrate with an increased propor-
In all biopsies the histologic sections showed a small and
tion of T- and B-cells in the connective tissue adjacent to the
well-defined inflammatory infiltrate in the connective tis-
barrier epithelium.6,8,10,16
sue lateral to the barrier epithelium. The lesions included
7.3% T-cells (CD3 positive) and 4.1% B-cells (CD19
Animal models
positive). Elastase-positive polymorphonuclear neutrophils
Experimental peri-implant mucositis models have evalu- (PMN) occured within the barrier epithelium and in the
ated the response of the peri-implant mucosa to both early connective tissue compartment immediately lateral to the
(3 weeks) and long-standing (90 days) periods of undisturbed barrier epithelium. The area of the inflammatory lesions
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.16-0488 by Readcube (Labtiva Inc.), Wiley Online Library on [22/01/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
HEITZ-MAYFIELD AND SALVI S261

corresponded to 0.36 mm2 , considerably larger than the implant. However, this study did not account for confound-
size of the lesions observed in the experimental short-term ing factors, and the reported association may have been due
(3 week) peri-implant mucositis study by Zitzmann et al.11 to the increased time in function without regular removal of
and histologic samples taken mainly from clinically healthy the biofilm.
sites.6,8 These studies confirmed the findings of Seymour Similarly, in a recent cross-sectional study conducted in
et al.21 who also evaluated biospies of nine subjects with 193 patients with implants in function for at least 12 months
long-standing peri-implant mucositis and found an increase in (range, 1 to 9 years), an association between peri-implant
size of the inflammatory lesion compared to clinically healthy mucositis and age and time of prosthesis in function was
sites.21 reported.34 However, a clear distinction between peri-implant
Peri-implant mucositis may be present for extensive peri- mucositis and peri-implantitis was not described. Ferreira
ods of time without progression to peri-implantitis. Conver- et al.34 also reported an association with peri-implant mucosi-
sion of the peri-implant mucositis lesion to peri-implantitis tis and systemic disease. However, the systemic diseases
in humans is difficult to study in an experimental design for described included “diabetes mellitus, hormonal changes,
obvious ethical reasons. However, in a longitudinal study of menopause, chemotherapy, thyroid alterations, cardiac prob-
patients diagnosed with peri-implant mucositis, those with a lems, and alcohol use,” and thus the results of the study are
lack of adherence to supportive peri-implant therapy had a difficult to interpret.
higher incidence of peri-implantitis at 5 years.22 Hence, sites
with peri-implant mucositis should be considered at increased
Major local risk indicators/factors
risk for the development of peri-implantitis.
Oral hygiene
Outcomes of cross-sectional clinical studies have clearly indi-
R ISK INDICATOR S/ FAC TOR S FOR cated that biofilm accumulation is associated with the pres-
PERI-IMPLANT MUCOSITIS ence of peri-implant mucositis around osseointegrated den-
tal implants.30,35,36 Ferreira et al.30 reported on 212 patients
At a previous World Workshop on Periodontology the def- treated with three different implant systems and diagnosed
inition of a risk factor was agreed as, “an environmental, with peri-implant mucositis. All implants had been in func-
behavioral or biologic factor confirmed by temporal sequence, tion for a period ranging from 6 months to 5 years. The
usually in longitudinal studies, which if present, directly modified plaque index37 was recorded, and the full-mouth
increases the probability of a disease occurring and, if absent plaque scores were stratified as good (median score ≤1), poor
or removed reduces that probability.”23 To identify a true risk (median score > 1 and < 2), and very poor (median score ≥2).
factor, prospective studies are required.24–26 The majority of The authors reported a significant dose-dependent associa-
studies available are cross-sectional or retrospective in design tion between plaque scores and peri-implant mucositis. The
and, therefore, in this review paper the term “risk” refers to prevalence of peri-implant mucositis was reported as 64.6%
a factor which is associated with peri-implant mucositis or a at patient level and 62.6% at implant level.30 Outcomes of
risk indicator. another study involving 218 patients with 999 implants in
function for a period of 9 to 14 years indicated that plaque
General risk indicators/factors scores were significantly associated with the presence of peri-
implant mucositis.35
Factors which may affect host susceptibility to biofilm- Mechanical biofilm control should be considered the stan-
induced peri-implant mucositis have been investigated. dard of care for management of peri-implant mucositis
Cigarette smoking has been identified as a risk indicator for administered either by the patient38 or the oral healthcare
peri-implant mucositis in three studies (Table 2).27–29 There professional.39
is also evidence for radiation therapy as a risk indicator for
peri-implant mucositis.27 There is some evidence for diabetes
mellitus as a risk indicator for peri-implant mucositis.28,30 Compliance/lack of compliance with supportive
Poorly controlled diabetes mellitus (HbA1c levels > 10.1) implant therapy (SIT)
was shown to be associated with increased bleeding on prob- Among patients not adhering to regular supportive implant
ing at implants.31 While a history of cardiovascular dis- therapy (SIT), peri-implant mucositis was reported to be a
aease has been associated with an increased risk of peri- common finding with a prevalence of 48% during an obser-
implantitis, there is no evidence for an association with peri- vation period of 9 to 14 years.28,35,40 Conversely, outcomes
implant mucositis.32 Máximo et al.33 reported a significant of a prospective cohort study with a 5-year follow-up indi-
but weak correlation (r = 0.44, Pearson 𝜒 2 test) between cated that implants placed in patients with treated periodon-
peri-implant mucositis and increased time of loading of the tal conditions and adhering to an SIT program yielded a
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.16-0488 by Readcube (Labtiva Inc.), Wiley Online Library on [22/01/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
S262 HEITZ-MAYFIELD AND SALVI

TABLE 2 Evidence for factors as risk indicators for peri-implant mucositis

Odds ratio (95%
CI), multivariate
Risk indicator Publication Summary analysis Significance
Plaque biofilm Roos-Jansaker 218 subjects, 9- to 14-year 1.9 (1.2 –2.9) P = 0.004
presence et al.28 follow-up, multivariate analysis
Plaque score: Ferreira et al.30 212 subjects all non-smokers, 1.9 (1.2 – 2.3) P = 0.0021
poor = median 6-month to 5-year follow-up,
plaque score > 1 multinomial regression analysis
and < 2
Plaque score: very Ferreira et al.30 212 subjects all non-smokers, 2.9 (2.0 – 4.1) P = 0.0027
poor = median 6-month to 5-year follow-up,
plaque score ≥2 multinomial regression analysis
Full-mouth plaque Konstandinitis 186 subjects, minimum 5-year 1.15 (1.01 – 1.33) P < 0.04
score 0.30 – 0.43 et al.36 follow-up, multilevel analysis
Full-mouth plaque Konstandinitis 186 subjects, minimum 5-year 1.36 (1.18 – 1.58) P < 0.001
score > 0.43 et al.36 follow-up, multilevel analysis
Periodontal Ferreira et al.30 212 subjects all non-smokers, 3.2 (2.0 – 3.3) P = 0.0025
BOP > 30% sites 6-month to 5-year follow-up,
affected multinomial regression analysis
Presence of Roos-Jansaker 218 subjects, 9- to 14-year 1.6 (1.1 – 2.3) P = 0.008
keratinized et al.28 follow-up, multivariate analysis
peri-implant
mucosa
Smoking Roos-Jansaker 218 subjects, 9- to 14-year 2.8 (1.2 – 6.2) P = 0.02
et al.28 follow-up, multivariate analysis
Smoking Karbach et al.27 100 subjects, 1- to 19-year 3.0 (1.14 – 7.92) P = 0.26
follow-up, cancer patients,
multivariate logistic regression
analysis
Smoking Rinke et al.29 89 subjects, mean observation 3.77 (1.2 – 11.86) P = 0.023
period 68.2 ± 24.8 months,
multiple logistic regression
analysis
Radiation therapy Karbach et al.27 100 subjects, 1- to 19-year 2.9 (1.08 – 7.83) P = 0.035
follow-up, cancer patients,
multivariate logistic regression
analysis
Male gender Ferreira et al.30 212 subjects all non-smokers, 1.7 (1.5 – 2.9) P = 0.0027
6-month to 5-year follow-up,
multinomial regression analysis
Diabetes Ferreira et al.30 212 subjects all non-smokers, NA NS
6-month to 5-year follow-up,
significant association in
univariate analysis but not in
multinomial regression analysis
Time in function Ferreira et al.30 212 subjects all non-smokers, NA NS
6-month to 5-year follow-up,
significant association in
univariate analysis but not in
multinomial regression analysis
Time in function Máximo et al.33 113 subjects, mean follow-up 3.4 NA NS
years, weak correlation Pearson
correlation coefficient (r = 0.44,
P = 0.0058)
NA, not applicable; NS, not significant; CI, confidence interval
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.16-0488 by Readcube (Labtiva Inc.), Wiley Online Library on [22/01/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
HEITZ-MAYFIELD AND SALVI S263

20% prevalence of peri-implant mucositis.41 In that study, management of peri-implant diseases. Implants with supra-
upon diagnosis of peri-implant mucositis, all implants with mucosal restoration margins yielded significantly greater
the exception of one were successfully treated according to reductions in probing depths following treatment of peri-
a cumulative anti-infective protocol.42 Findings from a 3- implant mucositis compared with those with submucosal
month randomized placebo-controlled clinical trial revealed restoration margins.43 This finding corroborates previous
that mechanical debridement with or without local applica- observations on the association between subgingival restora-
tion of chlorhexidine gel in conjunction with optimal self- tion margins at natural teeth and periodontal inflammation and
performed biofilm control completely resolved bleeding on attachment loss.51–53
probing around 38% of implants diagnosed with peri-implant Outcomes of a clinical retrospective study indicated that
mucositis.43 high proportions of implants diagnosed with peri-implantitis
In partially edentulous patients, pre-existing peri-implant were associated with inadequate biofilm control or lack of
mucositis in conjunction with lack of adherence to SIT was accessibility for oral hygiene measures, while peri-implantitis
associated with a higher incidence of peri-implantitis during a was rarely detected at implants supporting cleansible prosthe-
5-year follow-up period.22 The outcomes of that study yielded ses or when proper biofilm control was performed.54 Con-
a 5-year incidence of peri-implantitis of 18.0% in the group sequently, oral hygiene instructions should be individually
of patients with SIT and of 43.9% in the group without SIT, adapted to patients treated with dental implants because
respectively.22 The logistic regression analysis revealed that peri-implant mucositis may be considered a precursor for
lack of adherence to SIT within the overall patient sample peri-implantitis. Furthermore, whenever possible, margins of
was significantly associated with the onset of peri-implantitis implant-supported prostheses should be placed at or above the
with an odds ratio of 5.92.22 Hence, therapy of peri-implant peri-implant mucosal margin to facilitate access for biofilm
mucositis should be considered a prerequisite for the preven- control. Implant-supported reconstructions impairing access
tion of peri-implantitis. for biofilm removal should be adjusted or replaced by clean-
sible prostheses.

Materials and surface characteristics of implant

components Dimensions of keratinized peri-implant mucosa
Evidence for the influence of implant surface roughness on the The effect of the dimensions of peri-implant keratinized
incidence of peri-implant mucositis in humans is limited.44 A mucosa as a risk indicator for peri-implant mucositis was
12-month comparative analysis in humans between machined investigated in several studies in humans. While some stud-
titanium abutments (Ra = 0.2 𝜇m) and highly polished ies reported higher rates of peri-implant mucositis at implants
ceramic abutments (Ra = 0.0 6 𝜇m) indicated that further lacking or surrounded by an inadequate width (<2 mm) of ker-
reduction in surface roughness had no impact on bleed- atinized mucosa,55–60 other studies found no association61–63
ing on probing (BOP) scores.45 A study in humans investi- or a postive association.28 Collectively, evidence for the
gated the association between abutment surfaces of varying presence or minimum width of keratinized mucosa around
roughness and the early inflammatory response of the peri- implants to maintain soft tissue health and stability remains
implant mucosa.46 Although a statistically significant differ- controversial. In clinical situations of adequate self-performed
ence among patients was observed with respect to biofilm biofilm control around implants, presence or grafting of kera-
accumulation on the abutment surfaces and inflammatory tinized mucosa to maintain peri-implant health does not seem
cells, no association was observed between the inflammatory to be essential.
response and abutment surface roughness after an observation
period of 4 weeks.46
Compared with implants and abutments made of titanium, Excess cement
more beneficial properties in terms of biocompatibility have Excess cement has been associated with clinical signs of
recently been claimed for implants and abutments made of peri-implant mucositis.44,64–66 Patients restored with single-
zirconium dioxide (ZrO2 ). It has to be noted, however, that in unit crowns with excess cement displayed more signs of
clinical studies no significant differences in BOP scores47,48 peri-implant mucositis compared with those restored with
or slightly higher BOP scores49,50 were reported around ZrO2 single-unit crowns without excess cement.64 In addition,
compared with titanium abutments. peri-implant mucositis was more prevalent in patients with
cemented prostheses compared with those with screw-
retained prostheses.65 Therefore, to avoid cement excess,
Design of implant-supported prostheses restoration margins should be located at or above the peri-
Accessibility for biofilm removal around implant-supported implant mucosal margin or restorations should be cemented
prostheses plays an important role in the prevention and on individualized abutments allowing proper cement removal.
 19433670, 2018, S1, Downloaded from https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.16-0488 by Readcube (Labtiva Inc.), Wiley Online Library on [22/01/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
S264 HEITZ-MAYFIELD AND SALVI

SIMILARITIE S A N D D I F F E R E NC ES loss. Peri-implant mucositis is primarily caused by a disrup-

BET WEEN RI SK tion of the host–microbe homeostasis at the implant–mucosa
I N D I CATOR S / FAC TOR S FOR interface and is a reversible condition at the host biomarker
PERIODONTA L D I SE A SE S V E R S US level. Optimal biofilm control in experimental peri-implant
PERI-IMPLANT MUCOSITIS mucositis studies may take longer than 3 weeks for com-
plete resolution at the clinical level. Factors associated with
A recent systematic review summarized potential risk indi- peri-implant mucositis include biofilm accumulation, smok-
cators for peri-implant mucositis and identified biofilm accu- ing, and radiation therapy. Regular supportive peri-implant
mulation and smoking as risk indicators.44 In addition, a therapy with biofilm removal is an important preventive strat-
cross-sectional study showed that plaque score was a risk indi- egy against the conversion of health to peri-implant mucositis
cator for peri-implant mucositis in a dose-dependent manner and also against the progression of peri-implant mucositis to
(Table 2).36 Data from the 2009–2012 National Health and peri-implantitis.
Nutrition Examination Survey (NHANES) identified cigarette
smoking as a modifiable risk indicator for all levels of peri- ACKNOW LEDGMENTS AND DISCLOSURES
odontitis severity.67 Uncontrolled diabetes, male gender, and
The authors report no conflicts of interest related to this
age were also identified as risk indicators for periodontal
review paper.
disease.67 Thus, there are similarities in risk indicators for
peri-implant mucositis and periodontal disease, although
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