DOI: 10.1111/prd.

12255

REVIEW ARTICLE

Maintenance therapy for teeth and implants

Andrea Mombelli
Division of Periodontology, School of Dental Medicine, University of Geneva, Geneva, Switzerland

Correspondence
Andrea Mombelli, Division of Periodontology, School of Dental Medicine, University of Geneva, Geneva, Switzerland.
Email: andrea.mombelli@unige.ch

KEYWORDS
cumulative interceptive supportive therapy, implant maintenance, long-term results, maintenance guidelines, mechanical instrumentation,
patient role, periodontal maintenance, risk factors, supportive therapy

1 | INTRODUCTION Maintenance after completion of active periodontal therapy and

Prophylaxis aims at disease prevention, as opposed to therapy.
Primary prevention involves promotion of health and protection from
risk; secondary prevention includes procedures to identify and
eliminate early stages of disease; and tertiary prevention addresses
the damage caused by disease and aims to maintain or improve the
residual function. In this chapter of Periodontology 2000 we focus on
preventive measures taken either after completion of active peri-
odontal therapy or after dental implant therapy. In these situations,
health, disease, and disability are states that are not always clearly
discernible. As they depend on definitions of what constitutes dis-
ease, it is difficult to differentiate true prophylaxis from treatment of
persisting or recurrent disease, hence the term “maintenance ther-
apy.” This discrimination may seem without practical consequence
but it is relevant when discussing the cost efficiency of preventive
health‐care measures. Contrary to common belief, for some diseases
it is actually more efficient to wait for symptoms rather than to act
preventively. For example, it has been reported that expenditure on
medications and dietary interventions to decrease high blood‐choles-
terol levels exceeds the costs of treating heart disease: primary pre-
vention had a favorable cost‐effectiveness ratio only in subgroups
with specific risk patterns.1,2 In the context of this review, one may
ask: “How does enforcement of zero dental plaque tolerance com-
pare to maintenance focusing on pockets > 4 mm with bleeding or
suppuration after probing?” Generally speaking, the measures most
worth exploring and investing in are those that promise substantial
health benefits at a reasonable cost to a sizeable part of the popula-
tion.3 At an individual level, however, primary prevention can be per-
ceived as an investment in quality of life. In addition, maintenance
care after extensive periodontal and implant therapy may have a bet-
ter cost‐effectiveness ratio than primary prevention because of the
presence of specific risks.
after dental implant therapy has three components (Figure 1):
• Measures taken by the patient: personal oral hygiene; avoidance
of environmental risks, such as tobacco smoke; and management
of systemic diseases, such as diabetes.
• Preventive procedures carried out by a dental health-care profes-
sional: removal of supragingival deposits and polishing; elimination of
plaque-retention factors, such as defective or ill-fitting restorations.
• “Supportive periodontal therapy” sensu strictu: interventions
addressing the cause, the physiopathological mechanisms, or the
sequelae of recurrent or residual disease, such as subgingival bio-
film, inflammation, or tooth movement and mobility.
2 | ETIOLOGY OF PERIODONTITIS AND
PERI‐IMPLANTITIS: IMPLICATIONS FOR
MAINTENANCE
Five lines of evidence indicate that bacterial biofilms on the surfaces
of teeth and implants play a predominant role in the development
and progression of periodontitis and peri‐implantitis4-6:
• Experiments in humans showed that the accumulation of bacterial
plaque on teeth and implants over several days caused inflamma-
tion in the adjacent gingiva (“experimental gingivitis,” originally
described by Löe et al7) and peri-implant mucosa.8,9
• Cross-sectional observations revealed distinct quantitative and
qualitative differences in the microbiota associated with healthy
and diseased periodontal or peri-implant tissues.10-12
• In animal experiments, the subgingival placement of ligatures
around teeth and implants induced shifts in the composition of
the local microbiota and was followed by destruction of periodon-
tal and peri-implant tissue.13-15

190 | © 2018 John Wiley & Sons A/S. wileyonlinelibrary.com/journal/prd Periodontology 2000. 2019;79:190–199.
Published by John Wiley & Sons Ltd
MOMBELLI | 191

Maintenance care

Therapy
Preventive measures Preventive procedures “Supportive periodontal
taken by the patient carried out by a dental therapy” sensu strictu
health-care professional

Personal oral hygiene Removal of supragingival Interventions addressing the

deposits and polishing cause, the physiopathological
Avoidance of environmental mechanisms, or the sequelae of
F I G U R E 1 The three components of risks, such as tobacco smoke Elimination of plaque-retention recurrent or residual disease,
maintenance after completion of active factors, such as defective or ill- such as subgingival biofilm,
periodontal therapy and after dental Management of systemic fitting restorations inflammation, tooth mobility
diseases, such as diabetes
implant therapy

• Interventional studies in patients with periodontitis or peri-implan-
titis showed beneficial effects of mechanical biofilm removal and
enhanced outcomes after therapy with adjunctive antibiotics.16-19
• Long-term observations after periodontal therapy indicated that
poor outcomes were often associated with the presence of large
20-24
amounts of plaque.
Based on this evidence, the following requirements for periodon-
tal and implant maintenance are suggested6:
• Avoid accumulation of large quantities of bacteria, on teeth and
implants, to prevent inflammation of gingiva and peri-implant
mucosa.
• Eliminate or control local ecological factors, which favor the
growth of potentially pathogenic microorganisms around teeth
and implants.
• Remove bacterial deposits on teeth and implants - a crucial step
in the therapy of periodontal and peri-implant infections.
Although the primary etiologic role of bacteria is broadly
accepted, it has become clear, in recent years, that the tissue
destruction seen in periodontitis, and possibly also in peri‐implantitis,
can be attributed largely to dysregulation of inflammatory pathways
and inadequate immune responses to the presence of bacteria.25-27
These responses, and their consequences, may be quite variable
among individuals over time, and even from site to site within one
28-31
person. It has been reported that in monozygotic and dizygotic
twins reared together, approximately half of the phenotypic variabil-
ity of adult periodontal disease can be attributed to hereditary fac-
tors.32 Nevertheless, research has not been able to identify distinct
genetic factors with a strong and reproducible effect on susceptibil-
ity to periodontitis33 or peri‐implantitis.34
Changes in local ecological conditions may trigger the expression
of virulence factors35 or promote shifts in the composition of the
endogenous microbiota that may become intolerable for host
tissues.36 Alternatively, changes in the local environment may induce
reactions in the host tissues, which, in turn, may induce changes in
the microbiota. The mixed anaerobic infections arising after place-
ment of subgingival ligatures around teeth or dental implants,13-15 or
in the presence of excess luting cement on submucosal implant sur-
faces,37,38 can be attenuated with antimicrobial agents. However,
stopping the destructive pathological process in tissue requires the
foreign body to be removed. As a consequence, the differential diag-
nosis of primary or recurrent periodontal and peri‐implant infections
must include the search for a possible underlying trigger, even if sup-
puration or a microbiological test positive for anaerobic bacteria sug-
gest a bacterial cause.39
Possible risk factors for periodontal diseases have been studied
extensively. For a recent summary on modifiable risk factors in peri-
odontitis, the reader is referred to volume 64, 2014, of Periodontol-
ogy 2000. The list comprises (but is not limited to) smoking,
diabetes, stress, and socioeconomic status. The strength of evidence
to recommend intervention as part of periodontal therapy and main-
tenance to control such factors is variable. An in‐depth discussion
goes beyond the scope of this chapter. The best evidence exists for
smoking. It includes multifactorial analyses identifying smoking as an
independent risk for periodontal attachment loss in a dose‐depen-
dent manner,40,41 longitudinal studies demonstrating a temporal
sequence from exposure to disease,42,43 intervention studies show-
ing differential outcomes of periodontal treatment according to
smoking status,44-47 evidence of a positive influence of smoking ces-
sation on periodontitis occurrence and periodontal healing,48 and
long‐term follow‐ups showing a higher risk for disease recurrence in
smokers.22,23,49 In a systematic review,50 smoking, age, and initial
prognosis of a tooth were found to be associated with tooth loss
during long‐term periodontal maintenance. Possible risk factors for
biologic complications of dental implants have also been evaluated.
Tobacco smoking and a history of periodontitis were associated with
a higher prevalence of peri‐implantitis51 and increased risk for
implant failure.52,53
192 | MOMBELLI
3 | GENERAL EVIDENCE FOR BENEFITS OF
MAINTENANCE CARE
Studies carried out in the 1980s have convincingly demonstrated
that long‐term stability after periodontal therapy is possible if
patients practice good oral hygiene and are included in a regular
maintenance care program.21,54-63 Conversely, studies from that era
also demonstrated that without efficient oral hygiene and without
maintenance care the beneficial effects of various periodontal thera-
pies would disappear.20,64-68 The impact of patient compliance on
tooth loss during supportive periodontal therapy has been confirmed
69
recently by a systematic review and meta‐analysis.
The type and frequency of maintenance care may influence the
incidence and severity of recurrent periodontal disease and biologic
complications of dental implants. Forty‐three patients
advanced periodontal disease were informed about the importance
of plaque in the etiology of periodontal disease. After surgical
treatment they were re‐examined every 6 months, but no profes-
sional maintenance care was provided. The clinical and radiographic
outcomes after 4 years suggested that good oral hygiene was more
70
important than regular professional intervention. One study
showed that a rigorous recall program during the first 6 months
after therapy, with visits every 2 or 4 weeks, followed by mainte-
nance care at 3‐month intervals, gave better clinical outcomes than
the 3‐month maintenance program only. Another study showed
that patients included in a recall program with 2‐month intervals
between visits for 2 years and 3‐month intervals thereafter, had
clearly better periodontal conditions at 6 years than patients sent
71
back to the referring dentists for maintenance care. Regarding
dental implants, as the evolution from peri‐implant mucositis to
peri‐implantitis may be gradual, maintenance therapy has the poten-
tial to intercept infection before the bone has been damaged
extensively. In fact, patients who were included in maintenance
care programs in several long‐term studies72-75 showed occasional
symptoms of peri‐implant mucositis or early peri‐implantitis. Minor
problems were addressed with simple, nonsurgical interventions. In
these patients, advanced peri‐implantitis was a very rare outcome.
In another study with an 11% prevalence of peri‐implantitis at the
subject level,76 peri‐implant disease was never diagnosed in non-
smoking patients without a history of periodontitis and with good
compliance. A recent analysis of 13 studies reporting the incidence/
prevalence of biologic complications and the practice of aftercare
showed a significant effect of the interval of maintenance on the
incidence of peri‐implantitis.77
4 | MAINTENANCE AND THE RESIDUAL
POCKET
Even after the best clinically possible suppression of the pocket
microbiota, not all deep lesions transform predictably into a sulcus
with physiological probing depth. For example, in a randomized clini-
cal trial,78 80 patients with moderate‐to‐advanced periodontitis were
treated nonsurgically, surgically, and with systemic metronidazole
and amoxicillin for 7 days. Six months after the end of active ther-
apy, the mean number of residual pockets > 4 mm with bleeding on
probing was 3 per patient. In another cohort of 172 patients,79 on
average 4 residual pockets > 4 mm were counted per patient upon
completion of active periodontal therapy. Longitudinal microbiologi-
cal monitoring of treated sites showed that basically the same
microorganisms that were present before therapy would again be
found after therapy if no measures were taken to inhibit the forma-
tion and maturation of a new biofilm. Dark‐field microscopy was
used in a classical study to demonstrate this after nonsurgical
mechanical treatment.80 If no measures of prevention were taken,
large numbers of spirochetes and motile rods reemerged within 4‐
8 weeks. Conversely, in patients rinsing twice daily with a 0.2%
with solution of chlorhexidine, and receiving professional tooth cleaning
once every 2 weeks, a sustained, pronounced reduction in the
motile segment of the subgingival microbiota was achieved. In
another study,81 the composition of the subgingival microbiota was
similar to that of periodontally healthy sites 1 week after scaling
and root planing, the first signs of a shift toward pretreatment con-
63
ditions were noticed after 3 weeks, and no differences from pre-
treatment levels could be seen after 3 months. In a more recent
study,82 dynamic changes in the subgingival microbiome were inves-
tigated using metagenomic shotgun sequencing in patients with peri-
odontitis, before and after treatment. Follow‐up clinical examination
of previously sampled sites supported the predictive power of the
microbiome profile on disease progression.
As an interpretation of these findings, one may conclude that
regular prophylactic measures are required to maintain the microbio-
logical state achieved by periodontal therapy. Personal oral‐hygiene
procedures interfere with formation of supragingival biofilm and
address the issue of recontamination of treated sites with microor-
ganisms from the oral environment. These procedures have, how-
ever, only limited effects on bacteria that have either regained
access to the subgingival area or that were never completely
removed from there.83-86 Thus, interventions to interfere with bio-
film formation in the subgingival area may be necessary at intervals
of a few weeks to prevent recurrence of disease in residual pockets.
Repetitive scaling and root planing with steel instruments may
induce substantial loss of tooth substance with time.87,88 It is there-
fore vital to explore and evaluate mechanical and nonmechanical
alternatives that are less aggressive than use of steel instruments,
yet efficient enough to remove the nonmineralized subgingival bac-
terial deposits that grow between 2 maintenance visits. In this con-
text it is critical to distinguish between prophylaxis in the sense of
biofilm control, supportive therapy addressing “refractory” disease
caused by the persistence of hard and firmly attached residues (such
as calculus) that transform tooth or implant surfaces into foreign
bodies, or recurrent infection resulting from the presence of virulent
pathogens. The local application of an antibiotic is inappropriate as a
prophylactic procedure and cannot permanently cure a situation
complicated by a foreign body reaction; however, it may be an
option for treating a contained infection.
MOMBELLI
5 | THE ART OF DOSING MAINTENANCE
Prophylaxis carries the risk of overtreatment. In primary prevention,
treatment is given to healthy persons, but not all would develop the
disease if left untreated. In the future, a personalized medicine
approach using genetic and other biologic data, together with
anamnestic information, may help to tailor preventive care to peo-
ple's individual risks and to modify protocols as hazards change. The
evidence currently available suggests that this approach is promising.
However, present knowledge is largely insufficient to make precise
clinical recommendations; for example, how to use certain products
(and the appropriate dose) or procedures on an individual basis.
Multivariate analyses of data from a retrospective cohort study with
over 5000 persons89 revealed association of tooth extraction during
the previous 16 years with diabetes, smoking, and number of
preventive visits, but there was no evidence that genetic tests for
polymorphisms in interleukin 1 genes had an effect on the risk for
tooth extraction. Two annual preventive visits were beneficial for all
patients, regardless of the findings of genetic testing for interleukin
1 polymorphisms.90
Biologic mechanisms that deal with accumulation of bacterial pla-
que are influenced by nonmodifiable factors and probably continue
to dysfunction after periodontal therapy. Therefore, after periodontal
therapy, frequent maintenance visits may be needed to ensure long‐
term stability. As mentioned, a 3‐month recall interval seems to pro-
vide stability after periodontal treatment in nearly all patients, while
intervals of more than 6 months increase the risk for disease recur-
rence. Several authors have made suggestions of how to customize
maintenance after periodontal therapy according to risk. It has been
recommended to visualize a person's individual risk for disease recur-
rence using a spider‐chart – a graph showing 6 variables, potentially
increasing the risk on axes, all starting from a single point in the mid-
91
dle. The variables are:
• The percentage of bleeding on probing.
• The number of residual pockets > 4 mm.
• The number of lost teeth.
• Loss of periodontal support in relation to the patient's age.
• Systemic and genetic conditions.
• Environmental factors, such as cigarette smoking.
Data suggesting an effect on risk for disease recurrence have been
presented for each of these criteria.92 The area of the polygon formed
by connecting the data values on each axis is assumed to represent
the overall risk of a person to experience disease recurrence. The rela-
tive contribution of each factor (ie, the scale on each axis), is, however,
not based on comprehensive multivariate modeling, and the nature of
interaction of these variables may not fit the assumption of area under
the curve. The predictive value of the periodontal risk‐assessment
diagram area on long‐term treatment outcomes has been studied to
some degree retrospectively.93 The effectiveness and efficacy of this
and similar aids94,95 to tailor the needs for supportive therapy on an
individual basis have not been fully established.
| 193
Following therapy, the value of microbiological tests on the
pocket microbiota to predict stability during maintenance is unclear.
Some studies suggest that the subgingival presence of putative
pathogens, such as Porphyromonas gingivalis, might indicate an
increased risk for future alveolar bone loss.96 The levels of such bac-
teria in subgingival plaque samples, however, correlate with easily
measurable clinical parameters, especially probing depth and bleeding
on probing,97 and the attributed risks may essentially represent the
risk of having a residual pocket. A longitudinal study showed a lim-
ited potential of microbiological tests, performed after nonsurgical
therapy, to predict clinical outcome 6 months later, but confirmed
the importance of good oral hygiene98: participants still showing
multiple sites with visible plaque after the hygienic phase had an
increased tendency for bleeding on probing 6 months after scaling
and root planing. Another study found that microbiological parame-
ters reflecting bacterial load were more indicative of a risk for dis-
ease progression over 2 years of periodontal maintenance than the
presence or absence of specific marker organisms.99
Matrix metalloproteinases and other proteins measurable in gingival
crevice fluid have been proposed as biomarkers with value for peri-
odontal diagnosis. Associations between the levels of these enzymes
and clinical conditions have been reported.100 Longitudinal monitoring
indicated potential for the level of matrix metalloproteinase‐8 in gingival
crevice fluid to predict poor treatment outcomes, especially in smok-
ers.101 However, multiple questions remain because of high variability
in the results obtained, issues with methods of analysis and interpreta-
tion,102 and the absence of a cost‐benefit evaluation.
Clearly, more research evaluating biologic and clinical aspects,
and assessing questions of practical use and economic value, is
needed to substantiate claims of single diagnostic criteria, biomark-
ers, or combinations of risk factors as useful tools to adapt mainte-
nance care to individual needs.
6 | THE MAINTENANCE PROTOCOL
Diagnostic procedures in maintenance are not necessarily identical
to those of an initial examination or those of a thorough reevalua-
tion. The time available for these assessments is limited and needs
to be used efficiently. Repetitive clinical assessments made during
maintenance should focus on recent change and new pathology.
Data may concern the person as a whole, a tooth or an implant, or a
site on a tooth or an implant. At the level of the person there should
be a brief reassessment of general health, medications, or other ther-
apy, and of the dental history since the last visit. Specific charts have
been designed to record a restricted set of tooth‐ and site‐specific
data. An example is shown in Figure 2. The clinician is advised to
pass a periodontal probe in the sulcus around each tooth and
implant, but to note only probing depths > 4 mm, sites that bleed
after probing, and sites with suppuration or other signs of active dis-
ease. In addition, defective restorations and caries are noted. In
other words, the clinician will examine all sites but will limit note‐
taking to sites needing more attention than simply supragingival
194 | MOMBELLI
cleaning. Radiographs should not be viewed as part of routine main-
tenance. The decision to request selective radiographic examinations
should be based either on a question that remains unresolved after
the clinical examination or viewed as an integral part of a through
reevaluation. According to current official recommendations “dentists
should only order radiographs when they expect that the additional
diagnostic information will affect patient care.”103
Once the assessments have been completed, each of the 3 com-
ponents of maintenance outlined in Figure 1 should be addressed.
Regarding the measures taken by the patient, the clinician should
discuss his findings with the patient and use this opportunity to
motivate the patient to improve oral hygiene practices. Instructions
for improvement of oral hygiene deficits should be adapted to the
individual situation.104 Current evidence advocates behavior change
counseling in the dental practice setting for smoking cessation.105
Next, the clinician should remove any soft and hard deposits (plaque,
calculus, and stains) from all teeth and implants. The critical part of
supportive periodontal therapy sensu strictu is subgingival biofilm
control in residual pockets, as discussed in the next section. Should
further therapy be required, for example to address caries or a
defective restoration, a subsequent appointment should be given.
Under ideal circumstances this should occur rarely. Maintenance
therapy should not be confounded with continuous repair. At the
end of the visit a decision needs to be made regarding if the recall
interval should be altered or kept. Given the lack of clinical valida-
tion of risk‐assessment tools for programming recall intervals, as dis-
cussed above, the following practice is recommended:
• Upon completion of periodontal and/or implant therapy, mainte-
nance care should start at a frequency of 3 months.
• The stability of the situation should be evaluated continuously,
and the recall frequency should be adapted individually based on
longitudinal monitoring. If the patient has an adequate level of
plaque control and the comparison of present with past measure-
ments indicates stability, the interval can be prolonged up to 6
months by increments of 1 month from visit to visit.
• In some cases a high recall frequency is needed only because of
the presence of a high local risk that affects a single tooth or a
few sites. The benefit of guarding a heavily compromised tooth
or implant in an otherwise healthy dentition should be weighed in
comparison with alternative solutions.
7 | BIOFILM SUPPRESSION IN RESIDUAL
POCKETS
Scaling and root planing is a procedure used to remove bacterial
deposits from tooth surfaces by scraping with sharp metal instru-
ments. Initial periodontal therapy aims at removal of a combination
of firmly attached calculus and biofilm. Scaling and root planing is a
procedure with proven efficiency for this purpose.106 However, scal-
ing and root planing is not ideal for biofilm control in supportive
therapy because each time it is carried out it also removes tooth
substance; repeated applications can cause significant damage to
hard tissue.87,88,107,108 Various mechanical and chemical alternatives
to scraping with steel curettes have been proposed to remove bio-
film. Methods for disinfecting periodontal pockets include the use of
antimicrobial rinses, ointments, gels, and sustained drug‐release
devices. Evidence for clinical benefits comes mainly from randomized
clinical trials testing a single administration adjunct against a further
109-111
round of scaling and root planing. Protocols of repeated
antibacterial intervention to maintain teeth with residual pockets
without extensive mechanical reinstrumentation have, however, not
been tested extensively. Because of the risk of inducing bacterial
resistance, repeated treatments with local antibiotics are not
advisable, but other antimicrobial principles may be an option.
The microbiological and clinical effects of a varnish containing 1%
chlorhexidine and 1% thymol, applied upon completion of periodontal
therapy, were studied over 12 weeks.112 While the plaque index
increased significantly at sites treated with the placebo varnish, no simi-
lar increase was observed at the test sites. Nonsignificant differences in
microbiological parameters were observed between test and control
sites. The benefit of repeated subgingival controlled release of
chlorhexidine from a gelatin chip on periodontal maintenance was stud-
ied in 595 persons recalled at 3‐month intervals.113 Whenever a resid-
ual probing depth of ≥ 5 mm was detected, a chip was placed. After 2
years, the residual pockets showed a mean decrease of 1 mm in prob-
ing depth, 23% of patients had at least 2 pockets showing a reduction
in probing depth of ≥ 2 mm, and probing depth was reduced to
< 5 mm in 59% of sites, suggesting that repeated adjunctive application
of chlorhexidine chips may be a beneficial way in which to deal with
residual pockets in the maintenance phase.
Photodynamic therapy has been suggested as an option for the
therapy of periodontitis. Photodynamic therapy is based on the princi-
ple that some chemicals, such as the thiazine dye, methylene blue, can
be activated by light of a specific wavelength to kill bacteria.114,115
The dye could be applied to the periodontal pocket with an irrigator
tip and irradiated with light from a laser using a light‐diffusing tip also
introduced into the periodontal pocket. Three systematic reviews116-
118
evaluated the benefit of photodynamic therapy in periodontics,
either as an independent mode of therapy or as an adjunct to scaling
and root planing. The results were nondefinitive and inconsistent
regarding the clinical and microbiological effects. The value of photo-
dynamic therapy may be greater in the context of supportive peri-
odontal therapy because, in this situation, one may assume that the
root surfaces have been scaled and planed previously, and thus the
presence of subgingival calculus should not be the main issue. We
compared the benefit of photodynamic therapy with diode soft laser
therapy and thorough scaling and root planing for treatment of resid-
ual pockets.119,120 All three treatments resulted in a significant clinical
improvement. Photodynamic therapy and conventional scaling and
root planing resulted in fewer persisting pockets after 6 months than
did application of diode soft laser therapy, and yielded better microbi-
ological results. The effects of photodynamic therapy, delivered either
once or twice in a 1‐week interval after a short ultrasonic debride-
ment, were studied in 28 patients with residual pockets undergoing
MOMBELLI
5 5
F I G U R E 2 Chart to record a restricted set of tooth‐ and site‐specific data in the maintenance visit. The clinician passes a periodontal probe
in the sulcus around each tooth and implant, but only notes probing depths (PD) of > 4 mm, sites that bleed after probing (BOP), and sites
with suppuration or other signs of active disease
periodontal maintenance treatment.121 Probing depths were signifi-
cantly reduced in all groups. One or two sessions of photodynamic
therapy had an additional benefit over ultrasonic instrumentation
alone. At month 6, none of the sites treated twice with photodynamic
therapy had persisting probing depths of > 4 mm with bleeding upon
probing, whereas some sites treated only once, and an even larger
number of sites treated with ultrasonic instrument alone, had probing
depths of > 4 mm with bleeding upon probing.
Using a specially designed nozzle that can be introduced into a peri-
odontal pocket, subgingival biofilm can be removed with a jet of com-
pressed air containing a lightly abrasive powder. “Subgingival
air‐polishing” with glycine powder was tested for the first time in 50
patients with residual pockets in an examiner masked, randomized split
mouth clinical trial. The treatment was well tolerated and appeared to
122
be safe. A randomized clinical trial of 12 months’ duration, with a 2‐
arm, within‐subject parallel design, evaluated repeated subgingival air‐
polishing, using erythritol powder containing 0.3% chlorhexidine, in
residual pockets.123 In this trial, 50 patients were monitored at an inter-
val of 3 months. At months 0, 3, 6, and 9, sites presenting with a prob-
ing depth of > 4 mm were subjected to subgingival air‐polishing or
ultrasonic debridement. Subgingival air‐polishing reduced the number
of pockets > 4 mm to a similar degree as ultrasonic debridement but
induced less pain. Between baseline and 12 months, no significant dif-
ferences in the frequencies (> 1000 and > 100 000 cells/mL) of six spe-
cies of microorganism were observed. At month 12, test sites were less
frequently positive than control sites for Aggregatibacter actinomycetem-
comitans at > 1000 cells/mL, and bacterial counts in test sites never
exceeded 100 000 cells/mL.
8 | THE SPECIFIC ISSUES OF IMPLANT
MAINTENANCE
Although the preservation of marginal bone height is considered
crucial for implant stability, the 0.1 mm threshold for annual
| 195
change in bone height, proposed as a success criterion in the
past,124 is below the resolution of sequential conventional
radiographs of an individual implant and can only be estimated
arithmetically. Diagnostic protocols for implant maintenance should
include sensitive clinical assessments to detect signs of infection
before a substantial part of the supporting bone is lost. The
distance between the soft tissue margin and a reference point on
the implant (measurement of soft tissue hyperplasia or recession),
probing depth, the bleeding tendency, and suppuration can easily
be assessed using a periodontal probe. It is, however, unclear
whether bleeding on peri‐implant probing as a single observation
indicates an increased risk for peri‐implantitis. A high frequency of
bleeding on probing, and a disproportionately low incidence of
clinically manifested peri‐implantitis in several studies75,125-128 sug-
gests a high rate of false positive results. Rather than recording
the presence of blood as yes/no after having fully inserted the
probe, the bleeding tendency can be assessed more subtly using
the modified sulcus bleeding index (scored as follows: 0, no bleed-
ing; 1, isolated bleeding spots; 2, blood forms a confluent red line;
and 3, heavy or profuse bleeding) after passing the instrument
along the mucosal margin.129 The progression from peri‐implant
mucositis to peri‐implantitis is gradual and may be slow. There is
therefore an opportunity in maintenance therapy to intercept peri‐
implant disease early, hereby preventing substantial damage of
peri‐implant tissues. Patients in several studies have been included
in maintenance care programs carried out according to the
method of cumulative interceptive supportive therapy.6 Based on
regular assessment of the presence of plaque, probing depth,
bleeding tendency, and suppuration, peri‐implant infections were
searched for and treated as early as possible. Various clinical pro-
tocols for prevention and treatment of peri‐implantitis have been
proposed, including mechanical debridement, the use of antiseptics,
and administration of local or systemic antibiotics. For a recent
comprehensive review the reader is referred to the publication by
Heitz‐Mayfield & Mombelli.16
196 | MOMBELLI
9 | CONCLUSIONS
Studies have convincingly demonstrated that long‐term stability after
periodontal and implant therapy is possible if patients practice good
oral hygiene, avoid risks (such as smoking), and are included in a reg-
ular maintenance care program. Maintenance after completion of
active periodontal therapy and after dental implant therapy has three
components: measures taken by the patient; preventive measures
taken by a dental health‐care professional; and supportive therapy
addressing the cause or sequelae of recurrent or residual disease.
Subgingival bacterial deposits may not mineralize between two main-
tenance visits to form calculus; therefore methods less aggressive
than scaling and root planing may be more appropriate for residual
pockets. Repetitive clinical assessments made during maintenance
should focus on recent change and new pathology. Given the lack of
clinical validation of risk‐assessment tools for programming recall
intervals, the stability of the situation should be evaluated continu-
ously, and the recall frequency should be adapted to individual
patients based on longitudinal monitoring.
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How to cite this article: Mombelli A. Maintenance therapy
for teeth and implants. Periodontol 2000. 2019;79:190–199.
https://doi.org/10.1111/prd.12255