DOI: 10.1111/prd.
12240
REVIEW ARTICLE
Nonsurgical therapy for teeth and implants—When and why?
Niklaus P. Lang | Giovanni E. Salvi | Anton Sculean
Department of Periodontology, University of Berne, Berne, Switzerland
Correspondence
Niklaus P. Lang
Email: nplang@switzerland.net
Funding information
Clinical Research Foundation (CRF) for the Promotion of Oral Health, Brienz, Switzerland
KEYWORDS
clinical outcomes, implants, laser therapy, mechanical debridement, nonsurgical, periodontology, teeth, therapy
1 | HISTORICAL PERSPECTIVES
At the end of the 19th century, it was accepted that the treatment
of periodontitis had to be tackled by surgical means.1 The paradigm
of periodontal disease etiology and pathogenesis was that of an
infection that had spread into the alveolar bone and hence the
infected tissues had to be eliminated surgically to achieve healing.
Consequently, first of all “radical” gingivectomies and, later on, flap
surgical procedures, were advocated.
Periodontal flap surgery started around 1910 and was associated
2 3
with Neuman in Berlin, Cieszynski in Lviv, and Widman in Stock-
holm.4 However, it is rather difficult to trace the original rationale
and techniques applied by the different authors and hence no single
clinician can be named as the “inventor” of the periodontal flap.
Between the second and ninth decades of the 20th century,
periodontal surgical procedures were propagated depending on the
rationale of the pathogenesis believed by the respective clinicians.
After a first era of flap surgery advocated by Neuman2 and Widman4
that was directed at the alveolar bone believed to be infected, it
was demonstrated that alveolar bony lesions were not infected, but
rather showed patterns of bone resorption.5 As a consequence, gin-
givectomies enjoyed a renaissance and partially replaced flap surgery
again.
Subsequently, in 1949, Schluger6 published his view on peri-
odontal surgery, including the principle of osseous resection deter-
6
mining the future outline of the soft tissues. As a consequence, flap
surgery was emphasized anew for the years to come.
In 1974, Ramfjord7 finally described his novel technique of the
modified Widman flap. Instead of pocket eradication through oss-
eous resection, he followed a completely different treatment ratio-
nale, applying pocket reduction or pocket closure by repair after
thorough debridement of the root surfaces. The root surface had to
Periodontology 2000. 2019;1–7. wileyonlinelibrary.com/journal/prd
be made “biologically acceptable” in order to initiate a healing
response that is characterized by pocket closure, with or without the
presence of a long junctional epithelium.
None of the various surgical modalities were validated for a long
time, and the opinion of clinicians propagating one technique or
another dictated periodontal therapy in various parts of the world.
This changed dramatically after the initiation of longitudinal stud-
ies on periodontal therapy, first initiated by the Michigan group,8
and subsequently by the Gothenburg group9 and the Nebraska
group.10 Yet, these studies predominantly compared clinical out-
comes of various surgical treatments such as gingivectomies, pocket
eradication therapy with osseous resection, reparative surgery lead-
ing to pocket closure, and subgingival curettage.
At the time, no comparison with the outcome of nonsurgical
therapeutic approaches was available.
2 | EMERGENCE OF THE NONSURGICAL
THERAPEUTIC CONCEPT
Until the mid‐1980s, periodontal therapy always included periodontal
surgery of one design or the other. Nonsurgical therapy alone was
never performed, and it was even considered malpractice to deprive
a periodontal patient from receiving periodontal surgery. Nonsurgical
therapy was considered a preparatory measure and hence incom-
plete therapy.
Finally, in 1981 and 1983, the Minnesota group published a ran-
domized controlled clinical trial11,12 in which periodontal therapy
including scaling and root planing plus open flap debridement was
compared with scaling and root planing alone. Seventeen subjects
with moderate‐to‐advanced periodontitis received thorough scaling
and root planing, as well as oral hygiene instruction. A modified
© 2019 John Wiley & Sons A/S. | 1
Published by John Wiley & Sons Ltd
2 | LANG ET AL.

Widman flap was then randomly performed for one‐half of each sub-
ject's dentition. Recall prophylaxis and oral hygiene reinforcement
were administered for 6 and a half years after completion of ther-
apy. This was the first direct comparison of a surgical therapeutic
approach with a nonsurgical therapeutic approach. As the long‐term
outcomes (regarding pocket reduction and maintenance of attach-
ment levels) were not significantly different for lesions with initial
probing depth up to 6 mm, nonsurgical therapy became an accepted
treatment option without the stigma of being malpractice.
Only in periodontal sites with initial probing depth of ≥7 mm
was pocket reduction significantly greater when scaling and root
planing was followed with open flap debridement, However, attach-
ment level was maintained, with or without the addition of a peri-
odontal flap, even in those deep sites.11
11,12
Indeed, the Minnesota studies initiated a paradigm shift in
periodontal therapy toward a nonsurgical approach.
This was further substantiated by studies that started assessing
the outcome of the nonsurgical preparatory phase of periodontal ther-
apy before the surgical interventions.13,14 Mean measurements for
pocket depths of 1‐3, 4‐6, and ≥ 7 mm before treatment were com-
pared with their posttreatment scores. Pocket depth decreased signifi-
cantly for pockets extending ≥4 mm apically to the free gingival
margin. Suprisingly, the majority of the reduction in probing depths
and the gain in clinical attachment levels could be attributed to the
nonsurgical (hygienic phase) of periodontal treatment rather than to
the surgical procedure performed after the hygienic phase.14 In the
category of 4‐6 mm probing depth, a mean difference in pocket depth
of 0.96 ± 0.47 mm (P < .0001) between pretreatment and posttreat-
ment observations was found, while for probing depths of ≥7 mm, the
mean difference was 2.22 ± 1.35 mm (P < .0001). Gains in attach-
ment levels amounted to about 50% of the changes in probing depths.
This study clearly demonstrates that the clinical severity of peri-
odontitis was significantly reduced 1 month following the hygienic
phase of periodontal therapy and hence the need for surgical pocket
treatment could only be assessed properly after completion of non-
surgical periodontal treatment. As a consequence, nonsurgical peri-
odontal therapy has to be considered a prerequisite and the basis
for any type of periodontal therapy.
3 | NONSURGICAL VS SURGICAL
trials of at least 12 months’ duration: “Is there a difference between
Open Flap Debridement (OFD, surgical debridement) or Scaling and
Root planing alone (SRP, nonsurgical debridement) in terms of treat-
ment outcomes?”.15
As the most relevant evaluation parameter for the outcome of
periodontal therapy would be tooth loss and require extremely long
follow‐up periods, surrogate end‐point criteria were chosen for the
assessment. These included resolution of gingivitis (bleeding on prob-
ing), probing depth reduction, and clinical attachment level changes.
Of 589 abstracts that could possibly be used to answer the
focused question, only 6 randomized controlled trials that met the
inclusion criteria of the focused question were identified (Table 1).
Only patient based changes, 12 months after therapy, were consid-
ered. A total of 235 subjects were analyzed.15
The meta‐analysis of these studies indicated that, in shallow pock-
ets of 1‐3 mm depth, 12 months following treatment, nonsurgical
therapy resulted in 0.5 mm less attachment loss (weighted mean dif-
ference = −0.51 mm; 95% CI: −0.74 to −0.29) than surgical therapy.
In pockets with initial probing depth of 4‐6 mm, scaling and root
planing resulted in 0.4 mm more attachment gain (weighted mean
difference = −0.37 mm; 95% CI: −0.49 to −0.26) and 0.4 mm less
probing depth reduction (weighted mean difference = 0.35 mm; 95%
CI: 0.23‐0.47) than surgical therapy.
However, in deep lesions of >6 mm probing depth, 0.6 mm more
probing pocket depth reduction (weighted mean difference =
0.58 mm; 95% CI: 0.38‐0.79), and 0.2 mm more clinical attachment
level gain (weighted mean difference = 0.19 mm; 95% CI: 0.04‐0.35)
were achieved from surgical therapy after initial nonsurgical therapy
compared with nonsurgical therapy alone.15 The meta‐analysis for
the sites with initial probing depth >6 mm is presented in Figure 1
in a forest plot. In the category of advanced lesions (≥7 mm), open
flap debridement has a significantly greater effect on stimulating gain
of clinical attachment level than scaling and root planing alone.
It is obvious that periodontal surgery may only contribute to
achieve better therapeutic outcomes in deep lesions, while in lesions
T A B L E 1 RCT's suitable for analysis
Studies included, Subjects n, Duration,
author (year)Ref. Methods age range (y) y Outcomes
Lindhe et al RCT, SM 15, 32‐57 2‐5 PPD, CAL,
(1982)59 GI, PlI

PERIODONTAL THERAPY Lindhe et al RCT, SM 15, 42‐59 5 PPD, CAL,

(1984)60 BoP, PlI
Pihlstrom et al RCT, SM 17, 22‐59 6.5 PPD, CAL,
The longitudinal studies performed during the 1980s by several
(1983)12 GI, PlI
groups of clinicians all incorporated a nonsurgical periodontal ther-
Isidor & Karring RCT, SM 16, 28‐52 5 PPD, CAL,
apy group as a control in their comparison with various additional
(1986)61 BoP, PlI
surgical techniques. Hence, a database was established that allowed
Ramfjord et al RCT, SM 90, 24‐68 5 PPD, CAL
comparison of the outcomes of nonsurgical therapy alone with those (1987)8
of nonsurgical therapy followed by surgical interventions. Kaldahl et al RCT, SM 82, 43.5 7 PPD, CAL
In the European Workshop on Periodontology in 2002, periodon- (1988)10
tal therapeutic concepts were discussed on the basis of systematic
BoP, bleeding on probing; CAL, clinical attachment level; GI, gingival
reviews. For nonsurgical therapy the following focused question was index; PlI, plaque index; PPD, periodontal probing depth; RCT, random-
to be answered on the basis of only randomized controlled clinical ized clinical trial; SM, split month.
LANG ET AL.
F I G U R E 1 Meta‐analysis, in a systematic review, of treatment with
nonsurgical periodontal therapy, either alone or with surgical
periodontal therapy.32 Superiority of additional surgical therapy on
attachment level gain is indicated (weighted mean = 0.2 mm). Results
focus on initial probing depths of > 6 mm in depth. Patient‐based
changes after at least 12 months are reported. CAL, clinical attachment
level; OFD, open flap debridement; PPD, periodontal probing depth
up to 6 mm, nonsurgical therapy may be equally effective in reduc-
ing probing depth and gaining attachment levels. Hence, it can be
assumed that nonsurgical therapy is much more effective than hith-
erto recognized. On the other hand, it is obvious that nonsurgical
periodontal therapy has to precede additional surgical therapy.
4 | THE CONCEPT OF “CRITICAL PROBING
DEPTH”
For long term maintenance of therapeutic outcomes, the clinical
levels of attachment maintained over the years may be the most
clinically relevant surrogate variable assessed.16 As longitudinal stud-
ies have documented no major differences in the longitudinal main-
tenance of clinical attachment levels between sites treated
nonsurgically and those treated surgically, the clinician may be inter-
ested to know when to treat nonsurgically and when to add surgical
interventions to obtain the best therapeutic outcomes.
In this clinical decision‐making process, the concept of “critical
16
probing depth” may be helpful for the pretherapeutic evaluation of
single cases. It should be realized, however, that this regression anal-
ysis using data generated as mean scores from a trial comparing
nonsurgical and additional surgical interventions for root debride-
16
ment. Hence, the concept may be a valuable decision‐making tool
indicating trends of therapeutic outcomes. “Critical probing depth”,
in relation to clinical attachment level change, has been calculated
for various therapeutic approaches, including nonsurgical and addi-
tional surgical modalities. The clinical attachment level change is
plotted against the initial (pretherapeutic) probing depth. Subse-
quently, regression lines are calculated. The point at which the
regression line crosses the horizontal axis (the initial probing depth)
| 3
is defined as the critical probing depth. This, in turn, means that the
critical probing depth indicates the probing pocket depth before the
respective therapy below which clinical attachment would be lost as
a result of the respective treatment procedure. On the other hand,
above the critical probing depth, the therapeutic procedure would
result in clinical gain of attachment.
As an example, Figure 2 presents the regression analysis for both
nonsurgical and additional surgical periodontal treatment according to
the outcomes of a randomized controlled clinical trial.16 The critical
probing depth is consistently found to be greater for the additional
surgical approach than for the nonsurgical therapy. The regression line
for the nonsurgical therapy (root planing alone) crosses the horizontal
axis at a critical probing depth of 2.9 mm. This, in turn, means that
nonsurgical therapy results in loss of attachment when the clinical
probing depth is, on average, 2.9 mm. Above this value, nonsurgical
therapy appears to result in clinical attachment gain.
For the additional surgical approach (modified Widman flap), the
critical probing depth is found to be 4.2 mm, indicating that surgical
interventions would only be beneficial for achieving clinical attach-
ment gain if lesions with a probing depth of at least 4.2 mm are
treated.
Comparison of both regression lines (ie, those for nonsurgical
therapy, either alone or with surgical therapy) shows that the lines
cross at a critical probing depth of 5.4 mm. Again, this means that
only lesions above a probing depth of about 5.5 mm would benefit
from additional surgical therapy, while sites with a shallower probing
depth clearly require only nonsurgical therapy.
In conclusion, it may be stated that periodontal lesions by and
large can be treated successfully with nonsurgical therapy and that
additional surgical interventions should only be considered above a
critical probing depth of 6 mm. This limits periodontal surgical proce-
dures to advanced lesions that, after a successful hygienic phase, still
yield a probing depth of at least 6 mm.
5 | MEAN SCORES VS SINGLE SITES
It is obvious that the clinician faces the fact that his pretherapeutic
decisions concern single sites as well, while the concepts mentioned
above are based on mean scores of studies performed. Also, it is evi-
dent that the therapeutic outcomes of periodontal therapy may or
may not be maintained over time, depending on the cooperation of
the patient, including his/her standard of personal oral hygiene, on
the one hand, and the supportive maintenance care offered to the
patient on the other.
Cohort studies on long‐term maintenance (14 years) have indi-
cated that, while the great majority of periodontal sites remain stable
for many years, a very small proportion of sites (<1%) in approxi-
mately 25% (15 out of 61) of the treated patients will experience
reinfection and further loss of attachment despite the provision of
adequate supportive care.17 These reinfections occurred irrespective
of either the duration since active periodontal therapy or the cate-
gory of probing depth of the sites. This indicates that reinfection of
4 | LANG ET AL.

GAIN (mm)
All teeth and surfaces

Alterations: baseline-reexamination 6 months

4

3 RPL = Scaling and rootplaning

MWF = Modified widman flap
N=758
2
N=790
1
Attachment level

1 2 3 4 5 6 7 8 9 10
Initial probing
–1 depth mm

–2
MWF F I G U R E 2 Critical probing depth.16
4.2 ± 0.2 Regression analysis after nonsurgical
–3 therapy (scaling and root planing [RPL])
RPL
2.9 ± 0.3 and after additional surgical therapy
5.4 mm (Modified Widman Flap [MWF]). The
–4
critical probing depth for RPL is 2.9 mm
and for MWF is 4.2 mm. However, the
–5 benefit of additional surgery is first
obvious in teeth with a probing depth of
LOSS (mm) >5.4 mm

well‐treated and maintained periodontal patients is rare and com-
pletely unpredictable. Only one‐third of those reinfected sites
(n = 15) occurred in deeper pockets; the remaining two‐thirds were
noted in shallower pockets (n = 28). Hence, it cannot be anticipated
that either nonsurgical or additional surgical therapy may provide
better long‐term prognostic outcomes.
A more recent cohort study, on the long‐term maintenance
18
(11 years) of patients with treated advanced periodontitis,
mented similar results. While the majority of patients were com-
pletely stable, about 40% of the patients experienced single sites
with reinfection. In that study, treated sites with residual probing
depths of ≥6 mm had a significantly higher risk for the respective
tooth to be lost than if the probing depth was <6 mm. This means
that therapy should aim to avoid a residual periodontal pocket of
≥6 mm. If this goal is reached with nonsurgical therapy, additional
surgery may be redundant. Likewise, additional surgery may have to
be considered in sites with residual probing depth of ≥6 mm with
the goal of eliminating such pockets.
6 | NONSURGICAL THERAPY OF PERI‐
IMPLANT DISEASES
6.1 | Peri‐implant mucositis
Peri‐implant diseases were defined as (i) inflammatory lesions around
implants without loss of supporting bone (ie, peri‐implant mucositis);
and (ii) peri‐implant mucositis with additional loss of supporting bone
(ie, peri‐implantitis).19
Clinical signs of mucosal inflammation may include bleeding on
probing, erythema, swelling, and suppuration. The onset of peri‐
implant diseases is characterized by the presence of etiological fac-
tors similar to those involved in the etiology of periodontal
diseases.20
docu- A cause‐effect relationship between experimental accumulation
of oral biofilms around dental implants and the development of
experimental peri‐implant mucositis has been demonstrated in
humans.21-24 Hence, mechanical control of oral biofilms around den-
tal implants should be considered as the standard of care in the
management of peri‐implant mucositis administered either by the
patient25 or by the oral healthcare provider.26
Peri‐implant mucositis is considered to be the precursor of peri‐
implantitis. Peri‐implant mucositis was reported to be common
among patients not adhering to regular supportive maintenance care,
in whom a prevalence of 48% was reported during an observation
period of 9‐14 years.27-29 In a longitudinal study of patients diag-
nosed with peri‐implant mucositis, those without adherence to sup-
portive maintenance care yielded a 43.9% incidence of peri‐
implantitis after 5 years compared with 18% in patients adhering to
maintenance care.30 The logistic regression analysis revealed that
lack of adherence to supportive maintenance care within the overall
patient sample was significantly associated with the onset of peri‐
implantitis (odds ratio = 5.92).30 Furthermore, outcomes of a
LANG ET AL.
prospective clinical trial indicated that implants placed in periodon-
tally treated patients who were adhering to a supportive mainte-
nance care program yielded a 20% incidence of peri‐implant
31
mucositis over a 5‐year follow‐up. All implants but one were suc-
cessfully treated for peri‐implant mucositis according to a cumulative
interceptive antiinfective protocol.32
Outcomes from a 3‐month randomized placebo‐controlled clinical
trial indicated that mechanical debridement in conjunction with opti-
mal self‐performed control of the biofilms, with or without adjunc-
tive application of chlorhexidine gel, yielded complete resolution of
bleeding on probing in around 38% of the implants diagnosed with
peri‐implant mucositis.33 Moreover, implants with supramucosal
restoration margins yielded significantly greater reductions in pocket
probing depths following treatment of peri‐implant mucositis com-
pared with those with submucosal restoration margins.33
Findings from a randomized placebo‐controlled clinical trial failed
to show significant differences between groups when mechanical
debridement, in conjunction with systemic azithromycin, was deliv-
ered for the treatment of peri‐implant mucositis.34 The 6‐month clin-
ical improvements observed in the azithromycin group were
attributed to improved plaque scores and antiinflammatory proper-
ties of the systemic antibiotic.34 Nevertheless, the outcomes of this
study do not justify adjunctive delivery of systemic antibiotics for
the management of peri‐implant mucositis.34
Hence, based on these findings, peri‐implant mucositis should be
considered a risk indicator for the development of peri‐implantitis,
and the management of peri‐implantitis should focus on mechanical
debridement in conjunction with optimal self‐performed removal of
35
oral biofilms.
6.2 | Peri‐implantitis
The classic concept of nonsurgical periodontal treatment includes
root surface debridement using mechanical instruments, optimal
self‐performed plaque control, and regular supportive periodontal
therapy. Based on the fact that both periodontal and peri‐implant
20
diseases share similar etiological factors, this concept should also
be applied to the nonsurgical treatment of peri‐implantitis.
Mechanical nonsurgical therapy of peri‐implantitis without
adjunctive measures, however, showed only modest improvements
and limited predictability in the resolution of mucosal inflamma-
36-39
tion. In order to achieve resolution of inflammation and arrest
further bone loss, decontamination of the implant surface is of criti-
cal importance. However, decontamination of the implant surface is
much more challenging than decontamination of tooth surfaces.
Findings of a case series, in which mechanical debridement in con-
junction with peri‐implant pocket irrigation with 0.5% chlorhexidine
and adjunctive systemic delivery of ornidazole for 10 days was per-
formed, yielded positive clinical and microbiological results following
40
nonsurgical treatment of peri‐implantitis up to 12 months. Beneficial
clinical and microbiological effects following nonsurgical therapy of
peri‐implantitis were also reported when local delivery of chlorhexi-
dine or antibiotics was added to mechanical debridement.41-44
| 5
Outcomes of a randomized clinical trial indicated that in patients
with optimal self‐performed plaque control, mechanical debridement
with adjunctive delivery of photodynamic therapy or local antibiotics
yielded comparable improvements in the treatment of initial peri‐
implantitis with respect to clinical, microbiological, and host‐derived
parameters after 6 and 12 months.45,46 Complete resolution of
mucosal inflammation, however, was not routinely achieved with
either adjunctive photodynamic therapy or local antibiotic delivery.
Improvements in clinical parameters following nonsurgical treat-
ment of peri‐implantitis were also reported after adjunctive implant
surface decontamination using an air‐abrasive device47 and diode48
or erbium,26,49 laser, respectively.
Collectively, however, limited and unpredictable outcomes should
be expected after nonsurgical mechanical decontamination of the
implant surface, with or without adjunctive measures. Hence, in
cases of moderate to advanced peri‐implantitis, nonsurgical therapy
alone may not yield the expected success, and a surgical approach
to the peri‐implantitis defect is indicated.
7 | USE OF PHOTODYNAMIC THERAPY IN
TREATMENT OF PERIODONTAL AND PERI‐
IMPLANT INFECTIONS
Photodynamic therapy, also called antimicrobial photodynamic ther-
apy, photoradiation therapy, phototherapy, photochemotherapy,
photo‐activated disinfection, or light‐activated disinfection, was first
introduced in medical therapy in 1904 as the light‐induced inactiva-
tion of cells, microorganisms or molecules. Photodynamic therapy
includes the use of visible light, usually by means of a diode laser
and a photosensitizer (a substance that is capable of absorbing light
of a specific wavelength and transforming it into useful energy). The
various components of photodynamic therapy are harmless when
used alone, but in combination they lead to production of lethal
cytotoxic agents that can selectively destroy cells.50
In the last decade, photodynamic therapy has been proposed as
a potential alternative to treat infections caused by microorgan-
isms.51,52 Its mechanism is based on the illumination of a photosensi-
tizer which is converted from the ground state to the triplet state,
thus leading to the generation of cytotoxic species, usually singlet
oxygen (1O2), which interacts with the surrounding molecules and
cells. As singlet oxygen cannot migrate further than 0.02 μm, it has
only a local effect and does not damage distant cells or organs.53
Several in vitro studies have revealed that light from various
types of laser, including helium/neon or gallium‐aluminum‐arsenide
lasers, in combination with appropriate photosensitizers, can lead to
significant reduction in the numbers and viability of both aerobic
and anaerobic bacteria and of inflammation.54-56
Results from clinical studies indicate that in patients with chronic
periodontitis, the application of photodynamic therapy following sub-
gingival scaling and root planing may result in statistically signifi-
cantly higher short‐term clinical improvements, evidenced by
reduced probing depth and/or bleeding on probing, compared with
6 |
scaling and root planing alone.57 However, in patients with aggres-
sive periodontitis, the additional application of photodynamic therapy
yielded fewer clinical improvements compared with the systemic
administration of amoxicillin and metronidazole.58 At present, no
data that compare the application of photodynamic therapy with use
of systemic antibiotics are available for patients with chronic peri-
odontitis. The results of one randomized controlled clinical study
indicate that photodynamic therapy may represent a possible alterna-
tive to local antibiotics in patients with incipient peri‐implantitis.45,46
The evidence available indicates that photodynamic therapy can
be recommended in maintenance periodontal or peri‐implant therapy
and should be used only in conjunction with subgingival mechanical
debridement. However, at present, the use of photodynamic therapy
cannot be recommended as an alternative to systemic antibiotics for
the treatment of aggressive periodontitis or severe cases of chronic
periodontitis.
ACKNOWLEDGMENT
This report has been supported by the Clinical Research Foundation
(CRF) for the Promotion of Oral Health, Brienz, Switzerland.
CONFLICT OF INTEREST
The authors declare no conflict of interest with the concepts or
products mentioned.
REFERENCES
1. Robicsek S. Ueber das Wesen und Entstehen der Alveolarpyorrhöe
und deren Behandlung. 23. Jahresbericht der Vereinigung Oesterre-
ichischer Zahnärzte, 1883.
2. Neumann R. Die radikal‐chirurgische Behandlung der Alveolarpy-
orrhöe. Vierteljahrsschrift für Zahnheilkunde. 1921;37:113‐147.
3. Cieszynski A, Diskussion zu W. Strucks vortrag “Die sanatorische
behandlung der alveolarpyorrhöe nach eigener methode”. Deutsche
Monatsschrift für Zahnheilkunde. 1914;32:575‐576.
4. Widman L. The operative treatment of pyorrhea alveolaris: a new surgical
method. Svensk Tandläkar Tidskrift 1918;1‐80. Stockholm, Löjdqvists.
5. Kronfeld R. The condition of the alveolar bone underlying periodon-
tal pockets. J Periodontol. 1935;6(1):22‐29.
6. Schluger S. Osseous resection‐ a basic principle in periodontal sur-
gery. Oral Surg Oral Med Oral Pathol. 1949;2(3):316‐325.
7. Ramfjord SP, Nissle RR. The modified Widman flap. J Periodontol.
1974;45(8):601‐607.
8. Ramfjord SP, Caffesse RG, Morreiason EC, et al. Four modalities of
operiodontal treatment compared over 5 years. J Clin Periodontol.
1987;14(8):445‐452.
9. Westfelt E, Bragd L, Socransky SS, Haffajee A, Nyman S, Lindhe J.
Improved periodontal conditions following therapy. J Clin Periodontol.
1985;12(4):283‐293.
10. Kaldahl WB, Kalkwarf KL, Patil KD, Dyer JK, Bates RE. Evaluation of
four modalities of periodontal therapy. Mean probing debth, probing
attachment level and recession changes. J Periodontol. 1988;59
(12):783‐793.
11. Pihlstrom BL, Ortiz-Campos C, McHugh RB. A randomized four‐
years study of periodontal therapy. J Periodontol. 1981;52(5):227‐
242.
LANG ET AL.
12. Pihlstrom BL, McHugh RB, Oliphant TH, Ortiz-Campos C. Compar-
ison of surgicaland nonsurgical treatment of periodontal disease. A
review of current studies and additional results after 61/2 years. J
Clin Periodontol. 1983;10(5):524‐541.
13. Hämmerle CH, Joss A, Lang NP. Short term effects of initial peri-
odontal therapy (hygienic phase). J Clin Periodontol. 1991;18(4):233‐
239.
14. Morrison EC, Ramfjord SP, Hill RW. Short term effects of initial non‐
surgical periodontal treatment (hygienic phase). J Clin Periodontol.
1980;7(3):199‐211.
15. Heitz-Mayfield LJ, Trombelli L, Heitz F, Needleman I, Moles D. A
systematic review of the effect of surgical debridement vs non‐surgi-
cal debridement for the treatment of chronic periodontitis. J Clin
Periodontol. 2002;29(Suppl 3):92‐102; discussion 160-162.
16. Lindhe J, Nyman S, Socransky SS, Haffajee AD, Westfelt E. “Critical
probing depth” in periodontal thersapy. J Clin Periodontol. 1982;9
(4):323‐336.
17. Lindhe J, Nyman S. Long‐term maintenance of patients treated for
advanced periodontal disease. J Clin Periodontol. 1984;11(8):504‐514.
18. Matuliene G, Pjetursson BE, Salvi GE, et al. Influence of residual
pockets on progression of periodontitis and tooth loss: results after
11 years of maintenance. J Clin Periodontol. 2008;35(8):685‐695.
19. Lindhe J, Meyle J, Group D of European Workshop on Periodontol-
ogy. Peri‐implant diseases: Consensus Report of the Sixth European
Workshop on Periodontology. J Clin Periodontol. 2008;35(Suppl
8):282‐285.
20. Heitz-Mayfield LJ, Lang NP. Comparative biology of chronic and
aggressive periodontitis vs. peri‐implantitis. Periodontol 2000.
2010;53:167‐181.
21. Meyer S, Giannopoulou C, Courvoisier D, Schimmel M, Müller F,
Mombelli A. Experimental mucositis and experimental gingivitis in
persons aged 70 or over. Clinical and biological responses. Clin Oral
Implant Res. 2016;28(8):1005‐1012.
22. Pontoriero R, Tonelli MP, Carnevale G, Mombelli A, Nyman SR, Lang
NP. Experimentally induced peri‐implant mucositis. A clinical study in
humans. Clin Oral Implants Res. 1994;5(4):254‐259.
23. Salvi GE, Aglietta M, Eick S, Sculean A, Lang NP, Ramseier CA. Rev-
ersibility of experimental peri‐implant mucositis compared with
experimental gingivitis in humans. Clin Oral Implants Res. 2012;23
(2):182‐190.
24. Zitzmann NU, Berglundh T, Marinello CP, Lindhe J. Experimental
peri‐implant mucositis in man. J Clin Periodontol. 2001;28(6):517‐
523.
25. Salvi GE, Ramseier CA. Efficacy of patient‐administered mechanical
and/or chemical plaque control protocols in the management of peri‐
implant mucositis. Asystematic review. J Clin Periodontol. 2015;42
(Suppl 16):187‐201.
26. Schwarz F, Becker K, Sager M. Efficacy of professionally adminis-
tered plaque removal with or without adjunctive measures for the
treatment of peri‐implant mucositis. A systematic review and meta‐
analysis. J Clin Periodontol. 2015;42(Suppl 16):13.
27. Roos-Jansaker AM, Lindahl C, Renvert H, Renvert S. Nine‐ to four-
teen‐year follow‐up of implant treatment. Part I: implant loss and
associations to various factors. J Clin Periodontol. 2006;33(4):283‐
289.
28. Roos-Jansaker A-M, Lindahl C, Renvert H, Renvert S. Nine‐ to four-
teen‐year follow‐up of implant treatment. Part II: presence of peri‐
implant lesions. J Clin Periodontol. 2006;33(4):290‐295.
29. Roos-Jansaker A-M, Renvert H, Lindahl C, Renvert S. Nine‐ to four-
teen‐year follow‐up of implant treatment. Part III: factors associated
with peri‐implant lesions. J Clin Periodontol. 2006;33(4):296‐301.
30. Costa FO, Takenaka-Martinez S, Cota LOO, Ferreira SD, Silva GL,
Costa JEE. Peri‐implant disease in subjects with and without preven-
tive maintenance: a 5‐year follow‐up. J Clin Periodontol. 2012;39
(2):173‐181.
LANG ET AL.
31. Renvert S, Samuelsson E, Lindahl C, Persson GR. Mechanical non‐
surgical treatment of peri‐implantitis: a double‐blind randomized lon-
gitudinal clinical study. I: clinical results. J Clin Periodontol. 2009;36
(7):604‐609.
32. Lang NP, Mombelli A, Tonetti MS, Brägger U, Hämmerle CH. Clinical
trials on therapies for peri‐implant infections. Ann Periodontol.
1997;2(1):343‐356.
33. Heitz-Mayfield LJ, Salvi GE, Botticelli D, Mombelli A, Faddy M, Lang
NP. Anti‐infective treatment of peri‐implant mucositis: a randomised
controlled clinical trial. Clin Oral Implants Res. 2011;22(3):237‐241.
34. Hallström H, Persson GR, Lindgren S, Olofsson M, Renvert S. Sys-
temic antibiotics and debridement of peri‐implant mucositis. A ran-
domized clinical trial. J Clin Periodontol. 2012;39(6):574‐581.
35. Salvi GE, Zitzmann NU. The effects of anti‐infective preventive mea-
sures on the occurrence of biologic implant complications and
implant loss: a systematic review. Int J Oral Maxillofac Implants.
2014;29(Suppl):292‐307.
36. Heitz-Mayfield LJ, Mombelli A. The therapy of peri‐implantitis: a sys-
tematic review. Int J Oral Maxillofac Implants. 2014;29(Suppl):325‐
345.
37. Karring ES, Stavropoulos A, Ellegaard B, Karring T. Treatment of
peri‐implantitis by the Vector system. Clin Oral Implants Res.
2005;16(3):288‐293.
38. Rodrigo D, Martin C, Sanz M. Biological complications and peri‐
implant clinical and radiographic changes at immediately placed den-
tal implants. A prospective 5‐year cohort study. Clin Oral Implant
Res. 2012;23(10):1224‐1231.
39. Suarez-Lopez del Amo F, Yu SH, Wang HL. Non‐surgical therapy for
peri‐implant diseases: a systematic review. J Oral Maxillofac Res.
2016;7(3):e13.
40. Mombelli A, Lang NP. Antimicrobial treatment of peri‐implant infec-
tions. Clin Oral Implant Res. 1992;3(4):162‐168.
41. Büchter A, Meyer U, Kruse-Losler B, Joos U, Kleinheinz J. Sustained
release of doxycycline for the treatment of peri‐implantitis: Ran-
domised controlled trial. Br J Oral Maxillofac Surg. 2004;42(5):439‐
444.
42. Mombelli A, Feloutzis A, Brägger U, Lang NP. Treatment of peri‐
implantitis by local delivery of tetracycline. Clinical, microbiological
and radiological results. Clin Oral Implant Res. 2001;12(4):287‐294.
43. Persson GR, Salvi GE, Heitz-Mayfield LJ, Lang NP. Antimicrobial
therapy using a local drug delivery system (Arestin®) in the treat-
ment of peri‐implantitis. I: microbiological outcomes. Clin Oral
Implants Res. 2006;17(4):386‐393.
44. Salvi GE, Persson GR, Heitz-Mayfield LJ, Frei M, Lang NP. Adjunc-
tive local antibiotic therapy in the treatment of peri‐implantitis II:
clinical and radiographic outcomes. Clin Oral Implants Res. 2007;18
(3):281‐285.
45. Bassetti M, Schär D, Wicki B, et al. Anti‐infective therapy of peri‐
implantitis with adjunctive local drug delivery or photodynamic ther-
apy: 12‐month outcomes of a randomized controlled clinical trial.
Clin Oral Implant Res. 2014;25(3):279‐287.
46. Schär D, Ramseier CA, Eick S, et al. Anti‐infective therapy of peri‐
implantitis with adjunctive local drug delivery or photodynamic ther-
apy: six‐month outcomes of a prospective randomized clinical trial.
Clin Oral Implant Res. 2013;24(1):104‐110.
| 7
47. Renvert S, Lindahl C, Roos-Jansåker AM, Persson GR. Treatment of
peri‐implantitis using an Er:YAG laser or an air‐abrasive device: a
randomized clinical trial. J Clin Periodontol. 2011;38(1):65‐73.
48. Mettraux GR, Sculean A, Bürgin WB, Salvi GE. Two‐year clinical out-
comes following non‐surgical mechanical therapy of peri‐implantitis
with adjunctive diode laser application. Clin Oral Implant Res.
2016;27(7):845‐849.
49. Schwarz F, Bieling K, Bonsmann M, Latz T, Becker J. Nonsurgical
treatment of moderate and advanced periimplantitis lesions: a con-
trolled clinical study. Clin Oral Invest. 2006;10(4):279‐288.
50. Von Tappeiner HJA. On the effect of photodynamic (fluorescent)
substances on protozoa and enzymes (in German). Archive der Klinis-
chen Medizin. 1904;39:427‐487.
51. Sharman WM, Allen CM, van Lier JE. Photodynamic therapeutics:
basic principles and clinical applications. Drug Discovery Today.
1999;4(11):507‐517.
52. Wilson M, Dobson J, Harvey W. Sensitization of oral bacteria to kill-
ing by low‐power laser radiation. Curr Microbiol. 1992;25(2):77‐81.
53. Moan J, Berg K. The photodegradation of porphyrins in cells can be
used to estimate the lifetime of singlet oxygen. Photochem Photobiol.
1991;53(4):549‐553.
54. Dobson J, Wilson M. Sensitization of oral bacteria in biofilms to killing
by light from a low‐power laser. Arch Oral Biol. 1992;37(11):883‐887.
55. Sigusch BW, Pfitzner A, Albrecht V, et al. Efficacy of photodynamic
therapy on inflammatory signs and two selected periodontopathogenic
species in a beagle dog model. J Periodontol. 2005;76(7):1100‐1105.
56. Soukos NS, Mulholland SE, Socransky SS, et al. Photodestruction of
human dental plaque bacteria: enhancement of the photodynamic
effect by photomechanical waves in an oral biofilm model. Lasers
Surg Med. 2003;33(3):161‐168.
57. Sgolastra F, Petrucci A, Severino M, et al. Adjunctive photodynamic
therapy to non‐surgical treatment of chronic periodontitis: a system-
atic review and meta‐analysis. J Clin Periodontol. 2013;40(5):514‐526.
58. Arweiler NB, Pietruska M, Pietruski J, et al. Six‐month results follow-
ing treatment of aggressive periodontitis with antimicrobial photody-
namic therapy or amoxicillin and metronidazole. Clin Oral Invest.
2014;18(9):2129‐2135.
59. Lindhe J, Westfelt E, Nyman S, Socransky SS, Heijl L, Bratthall G.
Healing following surgical/non‐surgical treatment of periodontal dis-
ease. A clinical study. J Clin Periodontol. 1982;9(2):115‐128.
60. Lindhe J, Westfelt E, Nyman S, Socransky SS, Haffajee AD. Long‐
term effect of surgical/non‐surgical treatment of periodontal disease.
J Clin Periodontol. 1984;11(7):448‐458.
61. Isidor F, Karring T. Long‐term effect of surgical and non‐surgical
periodontal treatment. A 5‐year clinical study. J Periodontal Res.
1986;21(5):462‐472.
How to cite this article: Lang NP, Salvi GE, Sculean A.
Nonsurgical therapy for teeth and implants—When and why?
Periodontol 2000. 2019;00:1–7. https://doi.org/10.1111/
prd.12240