Treatment of aggressiveperiodontitisWIM TEUGHELS, RUTGER DHONDT, CHRISTEL DEKEYSER & MARC QUIRYNEN
Aggressive periodontitis comprises a group of rapidlyprogressing forms of periodontal disease that occurin otherwise clinically healthy individuals. It isaccepted that, compared with patients with chronicperiodontitis, patients with aggressive periodontitisshow a more rapid attachment loss and bonedestruction that occurs earlier in life. The patient’sage when attachment loss is detected is often thecriterion used by clinicians to diagnose aggressiveperiodontitis and to distinguish aggressive periodon-titis from chronic adult periodontitis [reviewed byAlbandar in this volume of Periodontology 2000 (3)].Typically, aggressive periodontitis runs in families(familial aggregation), pointing towards a geneticpredisposition. These three features (i.e. rapidattachment loss, bone destruction that occurs earlyin life and familial aggregation) are considered to bethe primary features of this disease. In the Workshopfor a Classification of Periodontal Diseases and Con-ditions, the secondary features of aggressive period-ontitis were identified as (i) relatively low amountsof bacterial deposits despite severe periodontaldestruction, (ii) presence of hyper-responsive macro-phage phenotypes, and (iii) increased portions ofAggregatibacter actinomycetemcomitans and Porphy-romonas gingivalis (46). Recently an entire volume ofPeriodontology 2000 was devoted to the differencesin clinical (5) and histopathological (93) features,epidemiological patterns (24), microbiological (4) andimmunological (29, 81) aspects, and genetic and envi-ronmental risk factors (94) between aggressive peri-odontitis and chronic periodontitis. From thesereviews it becomes clear that there are indeedmajor differences between aggressive periodontitisand chronic periodontitis. Despite these majordifferences, it is not always easy to differentiate thesetwo disease entities clinically. However, from aresearch perspective, it is essential that these diseasescan be, and are, clearly distinguished in order to gain
a complete understanding of their etiology andpathogenesis (5). Also, as pointed out throughoutthis review, from a treatment perspective, distinctionis of major importance. Additionally, patients withaggressive periodontitis are often diagnosed as havinga localized form or a generalized form of disease.Each form has its own typical clinical features. Therelative lack of clinical inflammation, often associatedwith the localized molar-and-incisor form ofaggressive periodontitis, has been recognized foralmost 100 years. It is generally accepted thatthis form of the disease is most often associated witha thin biofilm, at least in its early stages. In con-trast, the presence of clinical inflammation in gener-alized aggressive periodontitis appears to be similarto that observed in chronic periodontitis. In thissituation, age of onset and familial aggregation areimportant additional criteria for either diagnosis orclassification. It is also becoming more commonlyrecognized that chronic periodontitis may occursimultaneously with both localized and generalizedforms of aggressive periodontitis (reviewed in refer-ence 5).
The overall treatment concepts and goals inpatients with aggressive periodontitis are not mark-edly different from those in patients with chronicperiodontitis. Therefore, the different treatmentphases (systemic, initial, re-evaluation, surgical,maintenance and restorative) are similar for bothtypes of periodontitis. However, the considerableamount of bone loss relative to the young age ofthe patient and the high rate of bone loss warrantsa well-thought-through treatment plan and anoften more aggressive treatment approach, in orderto halt further periodontal destruction and regainas much periodontal attachment as possible. Theultimate goal of treatment is to create a clinicalcondition that is conducive to retaining as manyteeth as possible for as long as possible.
Printed in Singapore. All rights reserved PERIODONTOLOGY 2000
Diagnosis and treatment planning
Given the rapid progression of the disease and thehigh degree of difficulty in gaining control of thedisease, diagnosis and treatment of aggressive peri-odontitis should preferably be carried out by a peri-odontist. However, the general practitioner does playan essential role in the early detection of patientswho potentially have aggressive periodontitis. For aproper diagnosis, a thorough review of the patients’medical history, medications, family history andsocial history is required. In addition to an anamne-sis, screening tests can be performed to establishsystemic modifying factors such as diabetes andhematological conditions. Should a systemic diseasebe present, for instance poorly controlled diabetes,specialist medical consultation should be sought.Furthermore, risk factors, such as smoking and stress,must be identified.
The diagnosis should be made based on the above-mentioned criteria and considerations, together witha thorough mapping of the periodontal condition,which includes the recording of probing pocketdepths, clinical attachment levels, bleeding on prob-ing, furcation involvement, suppuration and toothmobility, and an assessment of the patients’ level oforal hygiene. These data, together with a radiologicalanalysis, are of utmost importance for screening andfor establishing the proper diagnosis and a differen-tial diagnosis. The diagnosis will also be a clear start-ing point for proper treatment planning, forevaluating and explaining treatment effects to thepatient and for patient education.
It is important to realize that even the most aggres-sive and advanced cases of periodontitis are treatable.Case reports have been published with a follow-up ofup to 19 years for patients with localized aggressiveperiodontitis (65) and a follow-up of up to 40 yearsfor patients with generalized aggressive periodontitis(67). However, it is essential for the patient to behighly compliant and highly motivated to do his partin order to gain control of the disease. A concertedeffort must therefore be made by the clinician toinform the patient about the severity of the diseaseand the risk factors, and the role of the patient in thetreatment. Also, the patient must be instructed veryprecisely about the necessary oral-hygiene measures.Furthermore, the clinician must assist the patient incontrolling risk factors, such as smoking.
Considerable evidence points to a familial aggrega-tion of aggressive periodontitis [discussed by Vieira &Albandar in this volume of Periodontology 2000 (104)].Therefore, it is the practitioners’ duty to inform the
patient of this aspect and at least suggest screeningother family members once the diagnosis has beenestablished. The patient should be asked about theperiodontal condition of their close relatives and, ifpossible, these relatives should seek consultation witha periodontist (11, 68).
Initial phase
Treatment of aggressive periodontitis starts withpatient education and ensuring patient compliance.A considerable amount of time should be invested inestablishing a good patient–clinician relationship.The time devoted to this, before commencing anyform of active treatment and during the whole pro-cess of periodontal therapy, will have an impact ontreatment success that should not be underestimated.The patient should be clearly informed about the dis-ease process, contributing factors, the differentphases and goals of the treatment, the predictabilityof treatment success and the patient’s own crucialrole in the treatment. The patient should be awarethat, for success, it is essential for optimal compliancein plaque control and maintenance and for possiblemodifiable risk factors to be addressed. If the cliniciandoubts the compliance of the patient, several pre-treatment visits could be included in the treatmentplan, in which compliance with oral-hygiene instruc-tions can be monitored and enhanced, together withcompliance towards, for example, a smoking-cessa-tion protocol.
Owing to the aggressive nature of the disease, clini-cians are often faced with teeth that are severely peri-odontally compromised. The prognosis of these teethneeds to be discussed with the patient when settingup a treatment plan (8). One of the most difficultaspects is whether or not to extract a tooth. It is oftenstated that retention of hopeless teeth, but also ofteeth with a doubtful prognosis, can compromise thetreatment outcome. Leaving residual pockets of� 6 mm is a risk factor for the progression of peri-odontal disease after active treatment (57). Residualdeep pockets are niches in the mouth where consid-erable numbers of pathogenic bacteria can remain,even after treatment. Earlier studies have reportedthe disappearance of pathogenic bacteria from themouth after extraction of compromised teeth, thuspreventing recolonization of other teeth (19). A pro-tective effect of extracting such compromised teethhas been identified in young children (78). It is there-fore suggested that a more radical extraction protocolis justified when treating patients with aggressive
Teughels et al.
108
periodontitis. However, the use of high-sensitivitybacterial-detection techniques has indicated thateven after a full-mouth tooth extraction, periodontalpathogens remain in the mouth. Van Assche et al.(100) performed a full-mouth tooth extraction in ninepatients and took microbial samples of subgingivalplaque, the tongue dorsum and the saliva beforeextraction, and samples of the tongue dorsum andthe saliva 6 months after extraction. Using a quantita-tive PCR analysis, the authors showed that, althoughtooth extraction resulted in significant reductions inthe numbers of periodontal pathogens, it failed toeliminate the pathogenic species from the mouth(100). A study by the same authors investigated themicrobial ecology in the newly formed pocketsaround implants placed in patients 3–6 months aftera full-mouth tooth extraction. They showed that assoon as 1 week after abutment connection, the detec-tion frequencies of pathogenic bacteria around thenewly placed implants had risen to detection fre-quencies comparable with those before extraction.The bacterial numbers, however, were lower thanbefore extraction (77). As a full-mouth extraction ofperiodontally compromised teeth does not result inthe elimination of pathogens from the mouth, theextraction of compromised teeth in the dentatepatient will probably not result in sufficient protec-tion from recolonization around other teeth. Thus,extraction of teeth should not be advocated for pre-venting colonization around other teeth in themouth.
Although the ultimate goal in the treatment ofaggressive periodontitis is to create a clinical condi-tion that is conducive to retaining as many teeth aspossible for as long as possible, this is obviously diffi-cult because patients with aggressive periodontitisare considerably younger than the average patientwith chronic periodontitis. This age aspect interfereswith treatment and treatment planning at differentlevels, some of which are not often considered.
One level is the psychological impact of the mes-sage that multiple teeth need to be extracted in youngpatients. Whilst there are currently no studies thataddress this aspect in patients with aggressive peri-odontitis, there are some indications that the impactof tooth loss on people and their lives should not beunderestimated. Davis et al. (20) reported that in acohort of 94 fully edentulous patients, 45% reportedretrospectively to have experienced difficulties inaccepting their tooth loss. In the cohort of Naik & Pay(66), which comprised 400 fully and partially edentu-lous patients, ‘only’ 25% of the patients reported hav-ing difficulties in accepting the loss of their teeth. One
of the major differences between both studies was theage of the patients, which was above 60 years in thestudy by Naik & Pay (66) but of a wider range(31 years and older) in the study by Davis et al. (20).It cannot be directly derived from the latter paperwhether younger patients experience more copingproblems than do older patients, but it could be areasonable hypothesis. Additionally, one should takeinto account that the patient’s attitude toward toothloss might be different in different parts of the world.Similarly, one could hypothesize that the compro-mised esthetics after periodontal therapy might havea significant effect on the general and psychologicalwell-being, self-esteem and daily social life of youngerpatients.
Another level on which age impacts treatment inaggressive periodontitis is the prosthetic rehabilita-tion. Obviously, when teeth are extracted, thepatient will seek adequate prosthetic rehabilitation.Although teeth can have a life expectancy of over80 years, there is currently no single type of pros-thetic device with a similar life expectancy. Thismeans that the age of the patient when a tooth/teeth are extracted can play a decisive role in thepatient’s quality of life. Early extraction of a puta-tively questionable tooth in a 40-year-old patientwith a life expectancy of 80 years could mean thestart of time-consuming and expensive prosthetictreatment for the next 40 years (30, 51, 74). How-ever, when considering that several studies havedemonstrated that compromised teeth can survivefor decades, given that a proper maintenance pro-gram is followed. In this regard, Graetz et al. (30)followed 34 patients with aggressive periodontitisand 34 patients with chronic periodontitis, whohad two or more teeth with alveolar bone loss of� 50%, for 15 years. After 15 years they found thatin the patients with aggressive periodontitis, 88.2%of the teeth with a questionable prognosis and59.5% of the teeth with a hopeless prognosis hadsurvived (30). These authors did not find any sig-nificant difference in tooth-survival rate betweenpatients with aggressive periodontitis and patientswith chronic periodontitis. It has been suggestedthat teeth with a predicted questionable prognosisas a result of severe bone loss should not be trea-ted periodontally, but rather extracted early toavoid possible involvement of neighboring teeth. Inregard to this aspect, it has been shown that long-term preservation of hopeless teeth is an attainablegoal with no detrimental effect on the adjacentteeth (53). The treatment of periodontally compro-mised teeth that have advanced bone loss is a
Aggressive periodontitis treatment
109
meaningful, therapeutic approach to prevent toothloss with the consequence of prosthetic rehabilita-tion. Several studies have been performed in whichthe prognosis of dental implants in periodontallyhealthy subjects has been compared with the prog-nosis of dental implants in subjects with aggressiveperiodontitis. De Boever et al. (21) placed implantsin, and followed up, 110 patients. Sixty-eight ofthese patients had suffered from chronic periodon-titis and 16 from generalized aggressive periodonti-tis. After a follow-up period of 100 months inwhich the patients were enrolled in a maintenanceprogram, there was a significant difference inimplant survival between the chronic periodontitisand generalized aggressive periodontitis groups,with implant-survival rates of 96% and 80%,respectively (21). Swierkot et al. (96) evaluated theprevalence of mucositis and peri-implantitis,implant success and implant survival in patientstreated for generalized aggressive periodontitis,over a period of 5–16 years, comparing them withperiodontally healthy subjects. They found thatpatients with generalized aggressive periodontitishad a five times greater risk of implant failure, athree times higher risk of developing mucositis anda 14 times greater risk of developing peri-implantitis(96). Similarly to these studies, Mengel & Floris-de-Jacoby (60) studied 39 patients over a 3-year per-iod following implant placement: 15 patients weretreated for generalized aggressive periodontitis, 12for chronic periodontitis and 12 patients were peri-odontally healthy. The results showed that theincrease in pocket depth and attachment loss wasgreater, and the implant-survival rate was lower, forsubjects with generalized aggressive periodontitisthan for periodontally healthy subjects or patientswith chronic periodontitis (60). From the aforemen-tioned studies it can be concluded that implant sur-vival in patients with generalized aggressiveperiodontitis is lower than in periodontally healthysubjects, or even in patients with chronic periodon-titis. For localized aggressive periodontitis specifi-cally there is very little evidence on which to baseany conclusions. Clinicians should be aware of thiswhen they consider implant-supported restorationsfor replacing teeth in patients with aggressive peri-odontitis, especially as patients with aggressiveperiodontitis are generally of a younger age than arepatients with chronic periodontitis. This means thatdental restorations need to remain functional andretain good esthetics for a longer period of time inthese patients. Consulting with other dental special-ists to assess the strategic restorative value of
certain teeth or to assess alternative restorativeoptions, such as orthodontic treatment, might helpin the final decision of whether to extract or toretain.
Active periodontal treatment
Despite better insights into the etiology of aggressiveforms of periodontitis, initial treatment is directedtoward the bacterial load in the periodontal pockets.As such, there is no difference between the treatmentconcepts used for treating chronic periodontitisor aggressive periodontitis. However, the clinicalresponse to nonsurgical therapy is much less docu-mented for aggressive periodontitis than for chronicperiodontitis. The number of studies assessing theeffect of periodontal treatment on aggressive peri-odontitis is limited and they often report on only asmall number of patients. This primarily relates to thelow prevalence of this disease, and this hampers theexecution of comparative clinical trials.
Nonsurgical therapy
Although the effect of nonsurgical treatment onchronic periodontitis is well documented (39), its effecton aggressive periodontitis is much less clear. In rela-tion to the effect of nonsurgical therapy alone as atreatment for aggressive periodontitis, two aspectsseem of importance. The first aspect relates to thequestion of whether, and to what extent, scaling androot planing alone can result in the desired clinicalchanges, such as probing pocket-depth reduction, gainin clinical attachment and reduction in bleeding onprobing. Ideally, this aspect is derived from data onthe magnitude of the effect on the clinical parameters(e.g. the amount of probing pocket-depth reduction)combined with data on the predictability (e.g. the pro-portion of patients responding to treatment). Unfortu-nately, the latter is often not reported. The secondaspect relates to the long-term stability of the resultsobtained. For this, longitudinal data are necessary.
For localized aggressive periodontitis, the effect ofnonsurgical therapy alone can be derived from stud-ies in which scaling and root planing represent thefirst phase of a staged combination therapy. In thisregard, Slots & Rosling (92), evaluated 20 deep pock-ets in six patients with localized aggressive periodon-titis and reported a small reduction of 0.3 mm in theprobing pocket depth 16 weeks after scaling and rootplaning. However, this reduction was accompaniedby a small average loss, of 0.05 mm, in clinical
Teughels et al.
110
attachment. Similarly to these observations, Korn-man & Robertson (44) reported an average probingpocket-depth reduction of 0.1 mm in eight patients,2 months after scaling and root planing. This virtualabsence of clinical response is, however, contradictedby data from comparative studies in which scalingand root planing alone represented the control treat-ment of the study. Reporting on 19 patients withlocalized aggressive periodontitis, Palmer et al. (72)showed an average reduction of approximately0.8 mm in probing pocket depth and an average gainin clinical attachment of approximately 0.3 mm forthe affected teeth, 3 months after scaling and rootplaning. Also, a reduction in bleeding on probing wasobserved. Asikainen et al. (6) even reported an aver-age probing pocket-depth reduction of 1.4 mm ineight patients, 2 months after scaling and root plan-ing. Unfortunately, none of the above-mentionedstudies performed a statistical analysis of theobserved effects. However, €Unsal et al. (99) analyzedthe clinical effect of scaling and root planing alone innine patients with localized aggressive periodontitisincluded in the control group of their study. Threemonths after performing scaling and root planing,pocket-depth reduction of 1.8 mm and clinicalattachment gain of 1.2 mm was recorded. Theseeffects were accompanied by a significant reductionin bleeding on probing, from 47.1% to 10.1%.Although the average probing pocket depth was notprovided by Sax�en et al. (83), it is interesting to notethat the four patients with localized aggressive peri-odontitis in the control group of the study who didnot receive surgery, showed a significant reduction inthe percentage of sites with a probing pocket depth of>4 mm, from 19.4% at baseline to 2.8% 20 monthsafter scaling and root planing. These findings are inline with those reported by Gunsolley et al. (35), whorecalled 19 treated and 21 untreated patients withlocalized aggressive periodontitis, approximately4 years after initial therapy. Some of the treatedpatients also received open flap curettage but,according to the authors, there was no significant dif-ference in response between both groups of treatedpatients. Although no statistical comparison betweenthe baseline and the recall data (approximately4 years after baseline) was performed, the clinicaldata show, for the treated patients, a reduction inprobing pocket depth of 0.2 mm and a gain in clinicalattachment of 0.3 mm. Interestingly, probing pocketdepth was increased by an average of 0.2 mm, and anadditional loss of attachment of 0.3 mm was recordedfor the untreated patients with localized aggressiveperiodontitis.
These limited data and statistical analyses on theeffect of scaling and root planing in patients withlocalized aggressive periodontitis hamper a solid con-clusion on its effectiveness and long-term stability.However, based on these data, it seems that scalingand root planing improves the clinical parameters inpatients with localized aggressive periodontitis, whichcontradicts the reports from the 1980s. Its predictabil-ity is unknown, but the clinical effects can berecorded for up to 3 years after treatment.
The effect of root planing alone on generalizedaggressive periodontitis is much better documented,although only one study has been specificallydesigned to assess the effect on clinical parameters.Hughes et al. (38) re-evaluated 79 patients with gen-eralized aggressive periodontitis, 10 weeks after scal-ing and root planing. They reported statisticallysignificant mean changes in overall probing pocketdepth of 0.4 � 1.7 mm, and of 2.1 � 2.0 mm for ini-tially deep pockets. An overall gain in clinical attach-ment of 0.2 � 1.93 mm was also recorded, and fordeep sites this was 1.77 � 2.15 mm. The percentageof bleeding on probing was reduced by 34%. Interest-ingly, the authors reported that 32% of the patientsdid not respond to treatment. Probably, this largeproportion of nonresponders can explain the largestandard deviation values observed in this study. Thenonresponding patients were primarily smokers. Theobservation that scaling and root planing indeedreduces clinical probing pocket depth and bleedingon probing, and results in a gain of attachment, isalso confirmed by several comparative studies inves-tigating the adjunctive effect of antimicrobials wherethe control group was treated with scaling and rootplaning alone (1, 7, 12, 34, 36, 37, 62, 76, 82, 88, 103,106, 107) (Table 1). These studies show averagewhole-mouth probing pocket-depth reductions rang-ing from 0.7 to 1.5 mm, and average gains in clinicalattachment ranging from 0.2 to 1.4 mm. For themajority of these studies the clinical changes werestatistically significant. These results confirm theeffectiveness of scaling and root planing in patientswith generalized aggressive periodontitis, at least forthe short term. In most of these studies the outcomeof scaling and root planing was assessed, for the firsttime, 2–6 months after the baseline measurementshad been performed. However, some studies followedthe clinical results over time, up to 24 months afterscaling and root planing, and the data from thesestudies can provide important information on the sta-bility of the clinical results obtained. The majority ofthese studies show that the probing pocket-depthreductions (1, 12, 36, 37, 88, 103, 107) and gains in
Aggressive periodontitis treatment
111
Tab
le1.
Summarytable
ofc
omparativestudiesusingad
junctivesystem
ican
tibiotics
inpatients
withge
neralized
aggressive
periodontitis
Study
(author
,ye
aran
dreference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Sigu
schet
al.
2001
(88)
Gen
eralized
aggressive
periodontitis
Scalingan
drootplaning
infour
tofive
sessions
Full-mouth
rootplaning
intw
osessions
within
48h(3
wee
ksafter
completion
ofinitial
therap
y)
Control
10Probingdep
th(m
m)
5.9�
0.7
5.5�
0.7
4.6�
1.0
5.2�
0.7
Probingdep
thdee
p(m
m)
8.2�
1.0
8.1�
0.1
5.9�
1.2
7.0�
1.0
Clin
ical
attach
men
tleve
l(mm)
6.3�
0.8
6.0�
0.9
5.7�
1.0
5.9�
0.8
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Doxycycline
(200
mg/
day
)
8day
s12
Probingdep
th(m
m)
5.5�
0.6
5.4�
0.6
3.9�
0.8
4.2�
1.1
Probingdep
thdee
p(m
m)
8.6�
1.2
7.8�
1.1
5.2�
0.8
6.6�
0.9
Clin
ical
attach
men
tleve
l(mm)
6.0�
1.1
5.9�
1.0
4.8�
0.8*
5.1�
0.9
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Metronidazole
(100
0mg/day
)8day
s15
Probingdep
th(m
m)
5.8�
0.7
5.8�
1.0
3.6�
0.8*
3.2�
0.7
Probingdep
thdee
p(m
m)
8.1�
1.1
7.6�
1.0
3.6�
1.1*
3.3�
1.1
Clin
ical
attach
men
tleve
l(mm)
6.2�
1.0
6.0�
0.7
4.3�
0.7*
4.0�
1.1
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Clin
dam
ycin
(600
mg/day
)8day
s11
Probingdep
th(m
m)
5.7�
1.1
5.6�
0.8
3.5�
1.0*
3.4�
0.8
Probingdep
thdee
p(m
m)
8.4�
0.8
8.0�
1.0
4.2�
1.1*
3.6�
1.0
Clin
ical
attach
men
tleve
l(mm)
6.1�
1.0
6.4�
0.8
4.4�
1.0*
4.2�
0.9
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Teughels et al.
112
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Guerrero
etal.
2005
(34)
Gen
eralized
aggressive
periodontitis
Scalingan
drootplaning
in1day
+
chlorhexidine
rinse
twice
daily
for
14day
s
Placebo
7day
s21
Probingdep
th(m
m)
Datanot
included
asthey
report
on
chan
ges
Probingdep
thdee
p(m
m)
Clin
ical
attach
men
tleve
l(mm)
Bleed
ingon
probing(%
)
Metronidazole
(150
0mg/day
)Amoxicillin
(150
0mg/day
)
7day
s20
Probingdep
th(m
m)
Probingdep
thdee
p(m
m)
Clin
ical
attach
men
tleve
l(mm)
Bleed
ingon
probing(%
)
Aggressive periodontitis treatment
113
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Xajigeo
rgiou
etal.2
006
(106
)
Gen
eralized
aggressive
periodontitis
Scaling
androot
planingin
fourvisits
Ultrasonic
deb
ridem
ent
(6wee
ksafter
completionof
scalingan
droot
planing)
Control
11Probingdep
th(m
m)
4.2�
0.7
3.2�
0.6*
3.5�
0.8*
Data
derived
from
grap
hs.
Additional
datawere
provided
asch
ange
s
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.6�
0.7
3.8�
0.6*
4.1�
0.6*
Bleed
ingon
probing(%
)78
�37
33�
24*
15�
25*
Metronidazole
(150
0mg/day
)Amoxicillin
(150
0mg/day
)
7day
s10
Probingdep
th(m
m)
4.6�
1.0
3.4�
0.5*
3.1�
0.7*
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.0�
1.0
4.3�
0.9*
4.0�
1.3*
Bleed
ingon
probing(%
)87
�21
22�
18*
15�
14*
Doxycycline
(200
mgon
day
1;10
0mg/day
therea
fter)
14day
s10
Probing
dep
th(m
m)
4.2�
0.6
3.5�
0.7*
3.4�
0.8*
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.0�
1.4
4.4�
1.7*
4.2�
1.9*
Bleed
ingon
probing(%
)81
�25
24�
23*
14�
22*
Metronidazole
(150
0mg/day
)7day
s12
Probingdep
th(m
m)
4.7�
0.6
3.5�
0.5*(a)
2.9�
0.6*(a)
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.4�
1.3
4.6�
1.1*
4.1�
1.3*
Bleed
ingon
probing(%
)80
�36
29�
15*
21�
31*
Teughels et al.
114
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Haa
set
al.
2008
(36)
Gen
eralized
aggressive
periodontitis
Scalingan
drootplaningin
fourto
six
sessions
within
14day
s
Placebo
12Probingdep
th(m
m)
Not
determined
Not
determined
Not
determined
Probingdep
thdee
p(m
m)
7.5�
0.4
5.3�
0.4*
4.8�
0.4*
5.1�
0.4*
Clin
ical
attach
men
tleve
l(mm)
Not
determined
Not
determined
Not
determined
Not
determined
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Azithromycin
(150
0mg/day
)3day
s12
Probingdep
th(m
m)
Not
determined
Not
determined
Not
determined
Not
determined
Probingdep
thdee
p(m
m)
7.3�
0.6
4.9�
0.4*
3.9�
0.5*
4.3�
0.4*
Clin
ical
attach
men
tleve
l(mm)
Not
determined
Not
determined
Not
determined
Not
determined
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Mac
hteie
tal.
2008
(54)
Fivewith
loca
lized
aggressive
periodontitis
and24
with
generalized
aggressive
periodontitis
Scalingan
drootplaningin
foursessions
withwee
kly
interven
ing
intervals
under
cove
rage
ofa
ntibiotics
Doxycycline
(100
mg/day
,afteraload
ing
dose
of2
00mg)
30day
s15
Probingdep
th(m
m)
4.09
�0.1
3.37
�0.1
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.93
�0.3
4.02
�0.2
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Not
determined
Metronidazole
(750
mg/day
)Amoxicillin
(150
0mg/day
)
14day
s14
Probingdep
th(m
m)
4.29
�0.2
3.53
�0.2
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.93
�0.3
4.14
�0.2
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Not
determined
Not
determined
Aggressive periodontitis treatment
115
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Mestnik
etal.
2010
(62)
Gen
eralized
aggressive
periodontitis
Scalingan
droot
planingin
14day
s+
chlorhexidine
rinse
twice
daily
for
60day
s
Placebo
14day
s15
Probingdep
th(m
m)
4.1�
0.6
3.2�
0.6*(a)
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.2�
0.5
3.5�
0.5*
Bleed
ingon
probing(%
)63
.6�
21.3
12.5
�11
.7*
Metronidazole
(120
0mg/day
)Amoxicillin
(150
0mg/day
)
14day
s15
Probingdep
th(m
m)
4.3�
0.7
2.7�
0.5*(a)
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.5�
0.8
3.2�
0.5*
Bleed
ingon
probing(%
)77
.7�
19.7
12.2
�13
.0*
Yek
etal.
2010
(107
)Gen
eralized
aggressive
periodontitis
Scalingan
droot
planingin
twovisits
Placebo
7day
s16
Probingdep
th(m
m)
3.7�
0.7
2.5�
0.5*
2.5�
0.5*
Data
derived
from
grap
hs
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
3.3�
1.3
2.30
�1.16
*2.4�
1.1*
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Metronidazole
(150
0mg/day
)Amoxicillin
(150
0mg/day
)
7day
s12
Probingdep
th(m
m)
4.06
�0.6
2.7�
0.5*
2.6�
0.4*
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
3.8�
1.1
2.7�
1.1*
2.8�
1.3*
Bleed
ingon
probing(%
)Not
determined
Not
determined
Not
determined
Teughels et al.
116
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Baltacioglu
etal.2
011(7)
Gen
eralized
aggressive
periodontitis
Scalingan
droot
planing
in24
h
Placebo
12Probingdep
th(m
m)
4.9�
0.3
4.2�
0.2*(a,b)
2months
instea
dof
3months
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.5�
0.5
4.7�
0.6*(a,b)
Bleed
ingon
probing(%
)95
.0�
0.1
37.7
�0.1*
Metronidazole
(750
mg/day
)Amoxicillin
(750
mg/day
)
10day
s14
Probingdep
th(m
m)
4.9�
0.7
3.4�
0.4*(a,c)
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.3�
0.8
4.0�
0.5*(a,c)
Bleed
ingon
probing(%
)93
.6�
0.1
25.2
�0.1*
Doxycycline
(200
mg
onday
1;10
0mg/day
therea
fter)
14day
s12
Probingdep
th(m
m)
5.0�
0.6
4.0�
0.3*(b,c)
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.7�
0.8
4.6�
0.4*(a,c)
Bleed
ingon
probing(%
)95
.2�
0.1
36.6
�0.2*
Aggressive periodontitis treatment
117
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Helleret
al.
2011
(37)
Gen
eralized
aggressive
periodontitis
Scalingan
droot
planing
(one-stag
efull-mouth
disinfection)
in24
h+
within
1wee
kstart
additional
scaling
androotplaning
ove
r4-6wee
ks
Placebo
10day
s15
Probingdep
th(m
m)
4.9�
0.2
3.5�
0.2*
3.5�
0.2*
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.2�
0.2
4.4�
0.2*
4.4�
0.2*
Bleed
ingon
probing(%
)83
.6�
4.4
54.0
�6.4*
69.0
�5.3*
Metronidazole
(750
mg/day
)Amoxicillin
(150
0mg/day
)
10day
s16
Probing
dep
th(m
m)
5.2�
0.2
3.3�
0.1*
3.2�
0.1*
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.6�
0.3
4.1�
0.2*
4.1�
0.3*
Bleed
ingon
probing(%
)85
.0�
3.1
45.0
�3.7*
60.0
�4.7*
Varelaet
al.
2011
(103
)Gen
eralized
aggressive
periodontitis
Scalingan
drootplaning
(one-stag
efull-mouth
disinfection)
in24
h+
within
1wee
kstart
additional
scalingan
droot
planing
ove
r4-6
wee
ks
Placebo
10day
s15
Probingdep
th(m
m)
4.2�
0.2
3.3�
0.1*
3.3�
0.1*
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.6�
0.3
4.0�
0.2*
3.9�
0.2*
Bleed
ingon
probing(%
)81
�4.9
50.9
�3.8*
57.9
�4.9*
Metronidazole
(750
mg/day
)Amoxicillin
(150
0mg/day
)
10day
s16
Probingdep
th(m
m)
4.3�
0.2
3.1�
0.1*
2.9�
0.1*
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.9�
0.3
3.8�
0.2*
3.8�
0.2*
Bleed
ingon
probing(%
)85
.7�
3.6
41.4
�2.7*
45.1
�4.2*
Teughels et al.
118
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Aim
ettiet
al.
2012
(1)
Gen
eralized
aggressive
periodontitis
Scalingan
droot
planing
(one-stag
efull-mouth
disinfection)
in24
h+
chlorhexidine
rinse
twice
daily
for60
day
s
Placebo
7day
s20
Probingdep
th(m
m)
4.5�
1.1
3.4�
0.8*(a)
3.3�
0.8*(b)
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
5.0�
1.2
4.0�
1.1*
4.0�
1.0*(c)
Bleed
ingon
probing(%
)56
.2�
18.2
16.6
�5.0*(d)
15.5
�3.8*(e)
Metronidazole
(150
0mg/day
)Amoxicillin
(150
0mg/day
)
7day
s19
Probing
dep
th(m
m)
4.3�
1.1
2.8�
0.6*(a)
2.7�
0.6*(b)
Probingdep
thdee
p(m
m)
Not
determined
Not
determined
Not
determined
Clin
ical
attach
men
tleve
l(mm)
4.7�
1.1
3.4�
0.8*
3.3�
0.6*(c)
Bleed
ingon
probing(%
)61
.5�
17.7
9.3�
0.8*(d)
9.4�
0.6*(e)
Aggressive periodontitis treatment
119
Tab
le1.
(Con
tinued
)
Study
(author,
year
and
reference
number)
Typ
eof
patient
Initial
trea
tmen
tRetreatmen
tusingastag
edap
pro
ach
(tim
ebetwee
ninitial
trea
tmen
tan
dretrea
tmen
t
Treatmen
tgroups
Duration
Number
ofpatients
per
group
Clinical
data
Variable
Baseline
Retreatmen
t3monthsafter
baseline
6months
after
baseline
12months
after
baseline
24months
after
baseline
Rem
arks
Casarin
etal.
2012
(12)
Gen
eralized
aggressive
periodontitis
Scalingan
droot
planingin
1day
Placebo
7day
s12
Probingdep
thmoderate(m
m)
5.2�
0.3
3.5�
0.7*
3.7�
1.1*
Probingdep
thdee
p(m
m)
7.5�
0.6
4.5�
0.8*
4.1�
0.9*
Relativeclinical
attach
men
tleve
lmoderate
(mm)
7.8�
1.0
6.6�
1.0*
6.8�
1.4*
Relativeclinical
attach
men
tleve
ldee
p(m
m)
10.0
�1.3
7.8�
1.3*
7.5�
1.2*
Bleed
ingon
probing(%
)34
.3�
6.1
11.7
�2.9*
11.0
�3.0*
Metronidazole
(750
mg/day
)Amoxicillin
(112
5mg/day
)
7day
s12
Probingdep
thmoderate(m
m)
5.1�
0.2
3.2�
0.6*
3.5�
0.6*
Probingdep
thdee
p(m
m)
7.7�
0.9
3.8�
1.1*
3.6�
1.4*
Relativeclinical
attach
men
tleve
lmoderate(m
m)
7.5�
1.9
6.4�
2.1*
6.8�
1.4*
Relativeclinical
attach
men
tleve
ldee
p(m
m)
9.9�
1.6
7.4�
2.1*
7.7�
2.6*
Bleed
ingon
probing(%
)39
.3�
6.5
11.1
�3.3*
10.3
�2.0*
Dataarepresentedas
mea
n�
stan
darddev
iation.
(a),(b),(c),(d),e)
Statistica
llysign
ifica
ntintergroupdifference.
*Statistically
sign
ifica
ntdifference
from
baseline.
Teughels et al.
120
clinical attachment (1, 12, 34, 36, 37, 88, 103) remainstable or improve, up to 6 months after the initialtherapy (Table 1). However, in some studies, there isalready a small relapse in probing pocket-depthreduction (34, 82, 106) or a gain in clinical attachment(82, 106, 107) between 3 and 6 months after scalingand root planing. Studies with longer follow-up (36,88) show that after 6 months, probing pocket depthsstart to increase and the obtained gain in clinicalattachment starts to decrease (Table 1). These find-ings are again in agreement with those reported byGunsolley et al. (35) who recalled 28 treated and 20untreated patients with generalized aggressive peri-odontitis, approximately 4 years after initial therapy.Although no statistical comparison was performedbetween the baseline data and the recall data, theclinical data show an increase in probing pocketdepth of 0.3 mm and a loss in clinical attachment of0.4 mm for the treated patients.
Based on these observations, it seems that general-ized aggressive periodontitis responds well to scalingand root planing in the short term (up to 6 months).However, after 6 months, relapse and disease pro-gression is reported, despite frequent recall visits andoral-hygiene reinforcements.
Systemic antibiotics
Treating patients with aggressive periodontitis ischallenging. The disease responds less predictablyto conventional mechanical periodontal therapythan chronic periodontitis (11, 90), the disease pro-gression is rapid and severe and patients are gener-ally of a younger age. Hence, scientists andclinicians have been exploring adjunctive treat-ments to enhance the outcome, stability and pre-dictability of conventional mechanical therapy. Inview of the specific microbiological nature of bothtypes of aggressive periodontitis, the use of chemo-therapeutics and, more specifically, of systemicantibiotics, could play an important role in thetreatment of these diseases.
Although it is currently well established that anti-biotics should not be administered without priordisruption of the bacterial biofilm (64), at least twostudies have evaluated the effect of systemic antibiot-ics as the sole form of therapy in patients with local-ized aggressive periodontitis (17, 69, 70). Thesestudies show that tetracycline, systemically adminis-tered over a period of at least 6 weeks, in combina-tion with supragingival plaque control, decreased theprobing pocket depths and resulted in gains in clini-cal attachment for up to at least 24 months. In addi-
tion, this regimen may lead to some repair of thealveolar bone defects. These data were largelyconfirmed by Slots & Rosling (92) who administered1 g of tetracycline for 2 weeks after completion of aninitial phase of scaling and root planing. The scalingand root planing reduced the total subgingival bacte-rial counts and the proportions of certain gram-nega-tive bacteria, but no periodontal pocket became freeof A. actinomycetemcomitans, and the study reportedsmall clinical changes after debridement. However,the administration of tetracycline, 6 weeks followingscaling and root planing, and in the absence of a newphase of instrumentation, resulted in a gain in clinicalattachment level of 0.27 � 0.45 mm and suppressionof A. actinomycetemcomitans, Capnocytophaga andspirochetes to low or undetectable levels in all testperiodontal pockets. Although these were importantobservations in relation to our understanding ofaggressive periodontitis, and although they wererecently confirmed in patients with chronic periodon-titis using metronidazole and amoxicillin (50), newerdata do not validate the treatment approach that wasused in the latter study. There is currently a clear con-sensus that mechanical instrumentation must alwaysprecede antimicrobial therapy. One should firstmechanically reduce the subgingival bacterial load,which might otherwise inhibit or degrade the antimi-crobial agent. Furthermore, one should mechanicallydisrupt the structured bacterial aggregates that canprotect the bacteria from the agent (64). Insufficientconcentrations of the active agent may favor theemergence of resistant bacterial strains.
Surprisingly, little investigation has been carriedout into the adjunctive effect of systemic antibioticson the outcome of mechanical instrumentation inpatients with localized aggressive periodontitis. Thefirst reports can be traced back to the end of the1970s (91); however, few studies have focused specifi-cally on localized aggressive periodontitis. It is obvi-ous that this hampers our current understanding ofthe use of systemic antibiotics in the treatment of thispatient group. Furthermore, the approach, in termsof the set-up of the studies, the combination of differ-ent treatments used and the way of reporting data,was markedly different in these older papers fromwhat is now considered to be the standard. Evenmore importantly, the development and the expo-nential increase of antibiotic resistance over the pasttwo decades should increase our awareness that theantibiotic regimens used then might no longer be aseffective. It must be considered that the absence ofclinical trials addressing the issue of adjunctive sys-temic antibiotics in the treatment of localized
Aggressive periodontitis treatment
121
aggressive periodontitis does not reflect a lack ofinterest in this disease. However, the low prevalenceof localized aggressive periodontitis makes it hard tofind sufficient numbers of patients, which might be areason for this lack of new studies. On the other hand,this lack might reflect a publication bias owing to theabsence of any significant adjunctive effect of sys-temic antibiotics. There is therefore an urgent needfor new clinical trials addressing this issue.
Although the adjunctive effect of tetracycline onscaling and root planing was observed by Slots et al.in 1979 (91), the limited number of patients in thestudy does not allow a definitive conclusion to bereached. Kornman & Robertson (44) reported on theadministration of systemic tetracycline (1 g/day for28 days) as an adjunct to scaling and root planing,starting on the first day of scaling and root planing. Itis assumed from their article that scaling and rootplaning was completed within the 28-day period inwhich the patients were taking the systemic antibiot-ics. Although this study was not placebo controlled,the eight patients included served as their owncontrols because they received scaling and root plan-ing without tetracycline 2 months before receivingscaling and root planing supplemented with systemictetracycline. The authors concluded that scalingand root planing alone had essentially no effect oneither clinical or microbiological parameters. Themean probing pocket depth was reduced from8.0 � 1.1 mm to 7.9 � 1.1 mm in this study. How-ever, when scaling and root planing was repeated inconjunction with systemic tetracycline, an additionalmean reduction in probing pocket depth to6.4 � 1.3 mm was recorded.
Despite several reports on the adjunctive use of sys-temic antibiotics during periodontal treatment(including surgery) of localized aggressive periodonti-tis (45, 56, 84), none of these studies actually evalu-ated the effect of antibiotics relative to scaling androot planing alone. The first actual randomized pla-cebo-controlled study was published by Asikainenet al. in 1990 (6). Sixteen patients were randomizedinto a placebo group and a group that received sys-temic doxycycline at a loading dose of 200 mg anddoses of 100 mg daily for 14 days thereafter. Allpatients received scaling and root planing as part oftheir treatment. Scaling and root planing was per-formed over an 8-week period, although the systemicantibiotic or placebo was only used during the first2 weeks of the scaling and root planing. No signifi-cant differences were found between groups in prob-ing pocket depth and bleeding on probing, duringand at the end of the study.
These results encouraged the researchers to explorethe effect of other systemic antibiotics. Sax�en &Asikainen (83) randomized 27 patients into a placebogroup, a tetracycline group (1 g/day for 12 days) anda metronidazole group (600 mg/day for 10 days).Scaling and root planing was performed at baselineand was repeated at 3 months. At 6 months postop-eratively, the periodontal condition had improved inall groups. However, in the metronidazole groupthe percentage of pockets deeper than 4 mm wasreduced more than in the other groups. Additionally,only one patient was still positive for A. actinomyce-temcomitans, whereas in the tetracycline and controlgroups, four and six patients, respectively, were stillpositive for the bacterium. Whilst no statistical analy-sis was performed, the authors concluded that therewas a higher predictability of the treatment results ofscaling and root planing when the treatment was per-formed with adjunctive use of metronidazole thanwith tetracycline.
In contrast to these results, Palmer et al. (72) evalu-ated the effect of adjunctive tetracycline (1 g/day for14 days) in 38 patients. Scaling and root planing wasperformed within 7 days, and the antibiotics wereadministered starting from the last scaling and rootplaning session. Three months after baseline theimprovements in probing pocket depth, clinicalattachment level and bleeding on probing were sig-nificantly better in the tetracycline group. Theseresults, in relation to the whole study, which alsoincluded a surgical phase, led the authors to concludethat systemically administered tetracycline is a usefuladjunct in the nonsurgical treatment phase of local-ized aggressive periodontitis. However, administeringthe antibiotic at the surgical phase did not provideany further, statistically significant, advantage.
Tinoco et al. (98) evaluated the effect of metronida-zole (750 mg/day for 8 days) combined with amoxi-cillin (1500 mg/day for 8 days) as an adjunct toscaling and root planing in a randomized, placebo-controlled study involving 20 patients with localizedaggressive periodontitis. Although 1 year after treat-ment, both groups showed significant clinical bene-fits, patients who had received systemic antibioticsadjunctively showed better results regarding probingpocket depth, clinical attachment level, gingivalbleeding index and radiological bone fill.
As it seems, from the above-mentioned studies,that adjunctive systemic antibiotics improve the clini-cal outcome in patients with localized aggressive peri-odontitis, the question arises of whether the type ofantibiotic is of importance. This aspect was addressedby Akincibay et al. (2), who compared the clinical
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outcome of systemic doxycycline vs. systemic metro-nidazole combined with amoxicillin during scalingand root planing. They randomly divided 30 patientsinto two treatment groups. The first group received100 mg of doxycycline for 10 days and the secondgroup received 375 mg of amoxicillin and 250 mg ofmetronidazole three times a day for 10 days. Theyfound that both groups showed significant improve-ments in plaque index, gingivitis index, periodontalprobing depth and clinical attachment level values.The metronidazole plus amoxicillin group showedsignificantly more improvement in plaque index andgingivitis index. Although the authors reported nostatistically significant differences in probing pocketdepths and attachment levels between both groups atthe end of the study, there was at least a clear ten-dency for more improvement in the metronidazoleplus amoxicillin group.
In contrast to localized aggressive periodontitis, theeffect of systemic antibiotics as an adjunct to scalingand root planing in generalized aggressive periodon-titis has been subjected to many more randomized,placebo-controlled studies. Among a variety of anti-biotics that can be used and have been tested asadjuncts in generalized aggressive periodontitis, thecombination of amoxicillin and metronidazole isbecoming advocated to an increasing extent. Therationale behind combining both antibiotics hasfound its origin in the observation that A. actinomyce-temcomitans was resistant to tetracycline, the antibi-otic of choice in the 1990s (83, 105). The failure oftetracycline to suppress A. actinomycetemcomitans,together with in-vitro data showing the synergisticeffect of metronidazole and amoxicillin on A. actino-mycetemcomitans (73) instigated van Winkelhoff et al.(101) to study the efficacy of this antibiotic combina-tion to eliminate A. actinomycetemcomitans fromsubgingival sites. The combination of 250 mg of metro-nidazole and 375 mg of amoxicillin, three times a dayfor 7 days, as an adjunct to scaling and root planing,was found to be very effective in suppressing subgin-gival A. actinomycetemcomitans (101). Both microbio-logical and clinical effectiveness of this combinationtherapy has been shown for patients with chronicperiodontitis (86). Recently, Sgolastra et al. (87) per-formed a meta-analysis of the effectiveness of theadjunctive use of amoxicillin and metronidazole inpatients with generalized aggressive periodontitis andincluded six randomized, placebo-controlled clinicaltrials (7, 34, 62, 103, 106, 107) published up to Sep-tember 2011. The study results clearly showed anadjunctive effect of the amoxicillin–metronidazolecombination in patients with generalized aggressive
periodontitis. Despite the fact that the majority of theincluded studies individually failed to show a statisti-cally significant effect, significant mean differences inclinical attachment gain of 0.42 mm, pocket-depthreduction of 0.58 mm, bleeding on probing changesof 14.95% and gingival bleeding changes of 21.44%were calculated in favor of the antibiotics. It is inter-esting to note that the mean differences for clinicalattachment gain, probing pocket-depth reductionand bleeding on probing in patients with aggressiveperiodontitis were higher than the mean differencesreported in another meta-analysis by the sameauthors, which investigated the adjunctive effectof the amoxicillin–metronidazole combination inpatients with chronic periodontitis (86). This maysuggest that patients with generalized aggressiveperiodontitis benefit more from an adjunctive combi-nation therapy than do patients with chronic peri-odontitis. Since September 2011, two additionalrandomized, placebo-controlled clinical trials havelargely confirmed the outcome of the meta-analysisof Sgolastra et al. (1, 12). It should be noted that inthese studies, a variety of dosages for both antibioticswere used (between 750 mg and 1500 mg/day), aswere a variety of administration regimens in terms ofduration (between 7 and 14 days) and how scalingand root planing was performed (see Table 1). As nocomparative data are available, it is currently impos-sible to define a clear protocol. However, data areavailable on the optimal timing of the use of amoxicil-lin and metronidazole in relation to nonsurgicaltherapy. It has been suggested that patients withaggressive periodontitis should initially be treatedwith scaling and root planing alone and then be clini-cally monitored, and only in refractory cases shouldsystemic antimicrobial therapy be used as an adjunctto re-instrumentation (91). Thus, antimicrobials aremore likely to be used at the retreatment visit ratherthan as part of the initial therapy (31). Although thisis a reasonable approach, it can only hold if patientswho receive antibiotics at the retreatment show atleast the same benefits compared with those whoreceive the same regimen at the initial therapy.Recently, in a retrospective study (43) as well as in aprospective study (31), it has been shown that there isa clear clinical benefit of using antibiotics at the initialtherapy compared with using them at retreatment.
Despite the fact that the combination of metroni-dazole and amoxicillin has shown additional clinicalbenefits beyond those of scaling and root planingalone in patients with generalized aggressive peri-odontitis, it is still not clear whether this combinationis more effective than other antibiotics because few
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comparative studies have been performed. Siguschet al. (88) compared the effects of metronidazole,clindamycin and doxycycline with a control grouptreated without antibiotics. It should be noted thatthe antibiotics were used at retreatment as an initialscaling and root planing procedure had been per-formed 3 weeks before re-instrumentation and anti-biotic administration. The authors reported that theuse of metronidazole or clindamycin was more effec-tive in reducing probing pocket depth and gainingattachment compared with the control or the use ofdoxycycline, indicating the superiority of these twoantibiotics. Similarly, also using a retreatmentapproach, 6 weeks after initial therapy, Xajigeorgiouet al. (106) assessed the effect of adjunctive use ofmetronidazole plus amoxicillin, metronidazole aloneor doxycycline alone, compared with a control group.Presumably owing to the small number of patients ineach group, no statistically significant differencescould be shown. However, it is interesting to note thatfor probing pocket-depth reduction and clinicalattachment gain, the largest additional benefit afterretreatment was seen for the metronidazole aloneand metronidazole plus amoxicillin groups. A smallerbenefit was noted for the doxycycline group, and nobenefit of retreatment was seen for the control group(106). Similar results, albeit reaching statistical signifi-cance, were recently obtained by Baltacioglu et al. (7)when the antibiotics were administered at initial ther-apy. In a study comparing the effectiveness of theadjunctive use of metronidazole plus amoxicillin,doxycycline, or scaling and root planing alone, theauthors found that the combination of metronidazoleplus amoxicillin resulted in a significantly greaterprobing pocket-depth reduction and gain in clinicalattachment compared with the use of doxycycline orwith the control treatment. However, doxycyclinealso showed a statistically significant additional prob-ing pocket-depth reduction and clinical attachmentgain vs. the control. In contrast to these studies,Machtei & Younis (54) could not find differences inclinical outcome between patients receiving eithermetronidazole combined with amoxicillin or doxycy-cline as adjuncts to first-phase therapy. In their study,24 patients with generalized aggressive periodontitisand five patients with localized aggressive periodonti-tis were divided over the two test groups. Patientsreceived a quadrant-wise scaling and root planing atweekly intervals and were given oral-hygiene instruc-tions. They were placed into one of two treatmentgroups: 1500 mg/day of amoxicillin and 750 mg/dayof metronidazole for 14 days; or a 200-mg load-ing dose of doxycycline followed by 100 mg of doxy-
cycline, daily, for 30 days. During the 3-monthfollow-up period, patients were recalled biweekly fororal-hygiene reinforcement and motivation. Theauthors found that under these conditions, bothregimes provided clinical improvements and that thedifferences in the results between both groups werenot significant. However, it should be borne in mindthat the duration of the doxycycline therapy wasmuch longer than for the regimen with other anti-biotics.
Taking this limited number of comparative studiestogether, it appears that the adjunctive use of metro-nidazole plus amoxicillin, metronidazole alone orclindamycin in patients with generalized aggressiveperiodontitis results in more pronounced clinicalimprovements when compared with the use of doxy-cycline for a similar amount of time or with scalingand root planing alone.
Recently, the effectiveness of azithromycin in thetreatment of aggressive periodontitis was also tested.Compared with other antibiotics, azithromycin hasthe advantage of having a long half-life. As azithromy-cin only needs to be administered once a day for3 days, one could assume that patient compliancewould be better compared with other antibiotic regi-mens. Compliance to an adjunctive antibiotic regi-men seems to be an important aspect for the clinicaloutcome in aggressive periodontitis. In a retrospec-tive analysis, Guerrero et al. (33) demonstrated thatincomplete adherence to a metronidazole plus amox-icillin regimen resulted in significantly less probingpocket-depth reduction and less gain in clinicalattachment. Therefore, Haas et al. (36) compared theclinical effect of the adjunctive use of azithromycinwith scaling and root planing in aggressive periodon-titis. One year after treatment, a significant additional1 mm reduction in probing pocket depth and 0.7 mmgain in attachment was evident, which shows thepotential of azithromycin in the treatment of aggres-sive periodontitis. In this study, localized and general-ized periodontitis patients were pooled.
Local antimicrobials
Although there is a clear rationale for the use of localantimicrobials, which is based on the emerging anti-biotic resistance, the possibility to achieve maximumantibacterial concentrations and the reduction of sys-temic side effects, the effectiveness of local antimicro-bials in aggressive periodontitis has barely beeninvestigated. However, especially for localized aggres-sive periodontitis, the localized character and limitednumber of diseased sites would in theory favor their
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use. Surprisingly, hardly any study has investigated,in a controlled manner, the possible adjunctive effectof local antimicrobials in localized aggressive peri-odontitis. To the best of our knowledge, only €Unsalet al. (99) have performed a comparative study. Inthis study, 26 patients with localized aggressive peri-odontitis were randomized, after scaling and rootplaning, into a control group, a group receiving 1%chlorhexidine gel (subgingivally administered) and agroup receiving a 40% tetracycline gel (subgingivallyadministered). The local subgingival administrationof either of the two antimicrobial agents did not resultin a significant additional improvement of the clinicalparameters in these patients after the 12-week obser-vation period. The use of local antimicrobial agentshas also been tested in generalized aggressive peri-odontitis. However, only one study actually comparedthe adjunctive use of a local antimicrobial vs. scalingand root planing alone (82). In this study, the effect oftetracycline fibers was investigated, in a split-mouthdesign, over a 6-month follow-up period in 10patients with generalized aggressive periodontitis.The adjunctive use of tetracycline fibers resulted instatistically significant additional probing pocket-depth reductions of 0.6 mm and in gains of clinicalattachment of 0.7 mm, up to 6 months after therapy.On the other hand, the effect of local antimicrobialshas been compared with the effect of systemic antibi-otics in patients with generalized aggressive peri-odontitis. Purucker et al. (76) compared the effect oftetracycline fibers with systemically administeredamoxicillin/clavulanic acid over a 52-week period in28 patients. Both adjuvants were applied 15 weeksafter initial therapy (8 weeks after the completion ofinitial therapy) without additional scaling and rootplaning. Under these conditions, no statistically sig-nificant differences between either treatment modali-ties were recorded in probing pocket depth andclinical attachment level. A significant difference inbleeding on probing was recorded at week 54 in favorof the systemic antibiotic. The study authors statedthat, because of the relatively small number ofpatients included, the claim that both antibiotic treat-ment modalities are equivalent cannot be made.Moreover, based on the data described above, thetiming of usage of both antibiotic modalities mightnot have been optimal. Additionally, although thedata were not statistically analyzed in this way, whenthe event of antibiotic application (week 15, 8 weeksafter completion of initial therapy) is used as thebaseline, there seems to be at least a numerical ten-dency that the systemic antibiotic provided a betterclinical adjunctive effect for probing pocket depth,
clinical attachment level and bleeding on probingcompared with the local antibiotic modality. Simi-larly, Kaner et al. (41) recently compared the effect ofa chlorhexidine chip with systemically adminis-tered amoxicillin (1500 mg/day) plus metronidazole(750 mg/day), both applied 1 week after the comple-tion of scaling and root planing. Over the 6-monthobservation period, the results show that scaling androot planing plus adjunctive chlorhexidine chips pro-vided clinical improvements, but these were notmaintained in full over the entire observation period.In the chlorhexidine chip group, probing pocketdepth significantly increased again between 3 and6 months. Scaling and root planing plus systemicamoxicillin/metronidazole was more effective withregard to reduction of pocket depth and gain in clini-cal attachment.
In conclusion, in patients with aggressive periodon-titis, the adjunctive effects of local antimicrobials,which have been reported in the literature, do notseem to improve on the adjunctive effect of systemicantibiotics. Only for generalized aggressive periodon-titis has an adjunctive clinical effect for tetracyclinefibers compared with scaling and root planing alonebeen shown. How local antimicrobials compare withsystemic amoxicillin plus metronidazole with regardto both cost–benefit and effectiveness is currentlyunknown. Therefore, it seems plausible that the deci-sion to use this type of treatment modality should bemade on an individual basis rather than be evidence-based.
Surgical treatment of aggressiveperiodontitis
The diagnosis of aggressive periodontitis is oftenmade at an advanced stage of the disease, whichmeans that clinicians will have to treat severely com-promised teeth. Consequently, after initial nonsurgi-cal therapy, residual pockets will remain, and thesemay require surgical treatment. Surgery provides thepractitioner with direct access to root surfaces andfurcation areas, thus permitting a more thoroughdebridement. It has also been suggested that becauseA. actinomycetemcomitans can invade the pocket epi-thelium, placing itself out of reach of scaling and rootplaning, the removal of pocket epithelium can helpin controlling the disease. Furthermore, intrabonydefects can be addressed by either bone-recontouringor regenerative techniques. Although few studies havespecifically addressed surgery in aggressive periodon-titis, those that have often report positive results. If
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risk factors, such as smoking, can be controlled, thelevel of maintenance therapy is high and the patientis compliant, the outcome of periodontal surgery inaggressive periodontitis can be comparable with thatin chronic periodontitis. Different surgical techniquesare possible in patients with aggressive periodontitis.
Access surgery
The effectiveness of a modified Widman flap proce-dure in reducing probing pocket depths is shown inseveral small-sample-size studies. Christersson et al.(15) treated 25 deep periodontal lesions in sevenpatients with localized aggressive periodontitis usingone of three treatments: scaling and root planingalone; scaling and root planing with additional soft-tissue curettage; or modified Widman flap surgery.Microbiological and clinical effects were monitoredup to 16 weeks after treatment. The results showedthat scaling and root planing alone did not effectivelysuppress A. actinomycetemcomitans in periodontalpockets, whereas scaling and root planing combinedwith soft-tissue curettage and modified Widman flapsurgery did. Furthermore, the clinical response totreatment was significantly better for scaling and rootplaning combined with soft-tissue curettage and formodified Widman flap surgery (16). Lindhe & Liljen-berg (49) treated 16 patients with localized aggressiveperiodontitis by means of tetracycline administration,scaling and root planing and modified Widman flapsurgery, after which the patients were enrolled in amaintenance program for 5 years. Lesions at firstmolars and incisors in a group of patients withchronic periodontitis were treated in an identicalmanner and served as controls. The treatmentresulted in the resolution of gingival inflammation,gain of clinical attachment and bone refill in angularbony defects. The healing of the lesions in thepatients with aggressive periodontitis was similar tothe healing observed in patients with chronicperiodontitis (49). In another study, performed byMandell & Socransky (55), eight patients with local-ized aggressive periodontitis were treated using modi-fied Widman surgery and a doxycycline regimen.Twelve months after surgery the treatment had beeneffective in eliminating A. actinomycetemcomitansfrom the pockets and obtaining mean probingpocket-depth reductions of approximately 3.6 mm, aswell as a mean attachment gain of 1.3 mm (55). Asidefrom these aforementioned studies there are manycase reports in which modified Widman surgeryhelped to accomplish a stable periodontium (75, 80).Buchman et al. (10) enrolled 13 patients with aggres-
sive periodontitis in a prospective case series andreported gains in clinical attachment for up to 5 yearsafter initial treatment. Treatment consisted of a com-bination of scaling and root planing, together withaccess surgery, without osseous recontouring forpockets deeper than 6 mm. All patients receivedamoxicillin combined with metronidazole systemi-cally. A significant 2.3-mm gain in clinical attachmentwas recorded 3 months after therapy. These improve-ments were maintained for up to 5 years after treat-ment during which the patients were enrolled in asupportive periodontal-therapy program. In thisstudy, periodontal-disease progression was success-fully arrested in 95% of the initially compromisedlesions, whilst 2–5% experienced discrete or recurrentepisodes of loss of periodontal support (10).
Regenerative surgery
An alternative to access surgery to resolve residualperiodontal pockets is the use of regenerative tech-niques in an attempt to resolve intrabony defects.Many different techniques (such as bone grafting,guided tissue regeneration using membranes, the useof biologic modifiers and combinations of the above)have been developed over the years to regenerate ver-tical bone defects. These techniques were designedfor the regeneration of steep vertical defects and havevery specific indications, and their effectiveness isdependent on the defect morphology, tooth mobilityand furcation involvement. Poor results are expectedin the treatment of horizontal bone loss, furcationdefects and increased tooth mobility (18).
Bone grafting
Bone grafting can lead to regeneration by providing ascaffold for the ingrowth of bone. There are differenttypes of grafts. Autografts are grafts that are harvestedfrom the patient’s own body and as such do not causemuch tissue reaction during healing. Theoretically,the autograft contains viable bone cells, giving it oste-ogenic qualities aside from osteoconductive qualities.However, it has been shown that few bone cells sur-vive the harvesting procedure. The autograft is thegraft of choice when available, but there are limita-tions in obtaining it. Alternatives are allografts (e.g.freeze-dried bone allograft), xenografts (bovine orcorral derived) and alloplastic materials (e.g. bioactiveglass, hydroxyapatite and beta-tricalcium phosphate).Although case reports have been published on theirutility in patients with aggressive periodontitis (22, 28,95), very few controlled studies have been conductedusing adequate numbers of patients or in which
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treatments were compared. Using freeze-dried boneallografts, Yukna & Sepe (108) reported an averagedefect fill of 80% in 12 patients with localized aggres-sive periodontitis at re-entry after 12 months. In addi-tion to this study, using a split-mouth approach,Mabry et al. (52) demonstrated significantly greaterbone fill (mean = 2.8 mm) and resolution of osseousdefects (mean = 72.7%) in allogeneic freeze-driedbone-grafted osseous bone defects in 16 patients withlocalized aggressive periodontitis when comparedwith defects that were treated with debridement only.The best results were obtained when adjunctive sys-temic tetracycline was administered using the surgi-cal procedure. Evans et al. (27) evaluated a 4:1(volume by volume) ratio combination of beta-trical-cium phosphate/tetracycline, hydroxyapatite/tetracy-cline or freeze-dried bone allograft/tetracycline in asplit-mouth study of 10 patients with localizedaggressive periodontitis. At re-entry, significantdecreases in defect depth and pocket depth weredetected for each graft material. No significant differ-ences between the different grafting materials werefound in terms of hard-tissue or soft-tissue changes.However, a greater percentage of defect fill was dem-onstrated for hydroxyapatite/tetracycline comparedwith beta-tricalcium phosphate/tetracycline. Theresults of these studies show that the use of thesegrafting materials in combination with tetracyclinecan result in additional bone fill and resolution of theresidual osseous defects in patients with localizedaggressive periodontitis.
Guided tissue regeneration usingmembranes
Membranes are used to influence the ingrowth of dif-ferent tissues into intrabony defects. By holding offthe ingrowth of epithelium and connective tissue,cells from the periodontal ligament are allowed togrow into the defect, resulting in regeneration of theperiodontal attachment. There are nonresorbable andresorbable membranes. Nonresorbable membranesprovide a marginally greater attachment gain, but asecond procedure is necessary for removing them. Re-sorbable membranes are biodegradable and do notrequire a second procedure to remove them; however,they do cause a greater inflammatory response. Theuse of nonresorbable expanded polytetrafluoroethyl-ene membranes has been shown to be effective forregenerating intrabony defects in aggressive peri-odontitis in case reports (25, 61, 89, 109).
Using a split-mouth approach, Sirirat et al. (89) com-pared the effect of a polytetrafluoroethylene mem-
brane with osseous surgery in six patients withaggressive periodontitis. Whilst both treatments wereeffective 1 year following surgery, probingdepth reduction and clinical attachment gain weresignificantly greater in the polytetrafluoroethylenemembrane-treated defects than in the osseoussurgery-treated defects, reaching a mean probingpocket-depth reduction of 2.6 mm and a gain inclinical attachment of 2.2 mm. The base of thepolytetrafluoroethylene membrane-treated defectsshowed a significant increase in bone fill. Zucchelliet al. (109) treated similar intrabony defects in 10patients with localized aggressive periodontits and in10 patients with chronic periodontitis using titanium-reinforced polytetrafluoroethylene membranes. After1 year there were no significant differences in theamount of clinical attachment gain, reduction ofprobing pocket depth or increase in gingival recessionbetween chronic periodontitis and localized aggres-sive periodontitis groups. DiBattista et al. (25) treatedseven patients with intrabony defects on first molarsusing surgical debridement, polytetrafluoroethylenemembrane, polytetrafluoroethylene membrane withroot conditioning or polytetrafluoroethylene mem-brane plus root conditioning and composite graft,consisting of calcium-sulfate, freeze-dried bone allo-graft and doxycycline. A significant gain in attach-ment and bone fill was observed for all techniques.There were no significant differences in resultsbetween the techniques. The average gain in attach-ment for all sites combined was 3.2 mm. The numberof patients in relation to the number of tested treat-ments in this study is low and does not permit rea-sonable conclusions to be made on the effect of theseparate techniques. Mengel et al. (61) performed acomparative study on the regeneration of one- tothree-wall bony defects in 12 patients with general-ized aggressive periodontitis using a bioresorbablemembrane or with bioactive glass. They treated 22defects using a membrane and 20 defects using thealloplastic graft. Both treatment modalities resultedin significant changes in probing pocket depth and inclinical attachment gain of about 4 mm and 3 mm,respectively. No significant differences between thetwo treatments were found.
Biological modifiers
The use of enamel matrix proteins (amelogenin)attempts to recreate the physiological environmentfor the development of the periodontal ligament. Thisallows the regeneration of new cementum and theformation of new attachment in periodontal defects.
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The use of enamel matrix protein results in moreattachment gain than open-flap debridement inpatients with chronic periodontitis (26). There is,however, little evidence for an advantage in patientswith aggressive periodontitis. Most published articleson the use of enamel matrix protein in patients withaggressive periodontitis are case reports (9, 42). Inthis regard, Vandana et al. (102) published a case ser-ies involving four patients with chronic periodontitisand four patients with aggressive periodontitis. Six-teen intrabony defects were surgically treated witheither enamel matrix proteins or surgical debride-ment alone using a split-mouth design. The meanpocket-depth reduction and amount of defect fillwere significant in both treatments, 9 months post-surgery, in both groups of patients. No significant dif-ferences in mean pocket-depth reduction, clinicalattachment level gain, amount of defect fill or defectresolution were detected between the two treatments,in both groups of patients. This study failed todemonstrate an advantage of using enamel matrixproteins compared with surgical debridement alone.
Growth factors and differentiation factors also playan import role in tissue development and healing andare therefore used as tools for gaining attachment.Mediators such as platelet-derived growth factor,insulin-like growth factor, fibroblast growth factor,bonemorphogenetic protein and transforming growthfactor-beta have shown promising results in animalstudies and in vitro (71, 79, 97). Platelet-rich plasmahas been shown to improve clinical and radiographicparameters for compromised teeth (58). Their disad-vantages are the low tissue specificity and unknownsystemic effects. At present, their effectiveness inpatients with aggressive periodontitis is unknown(23, 80). There is, however, a case series published byMauro et al. (58) on the regenerative surgery of intrab-ony defects with platelet gel. Three patients, who hadshown a refractory response to previous treatments,were treated and followed for 15 months. The oper-ated sites showed a reduction of pocket depth and again in attachment. Moreover, the effect remained sta-ble during the 15-month follow up, whereas previoustreatments had not been as effective (58).
Maintenance therapy
Once treatment has resulted in a stable and healthyperiodontium, the patient should enter a mainte-nance program. The purpose of this supportive peri-odontal therapy is to ensure that periodontal healthis maintained after active therapy (40), so that no
additional teeth are lost and disease recurrence isprevented. Supportive periodontal therapy shouldtherefore be directed towards risk factors for diseaserecurrence and tooth loss. Several factors (such assmoking, diabetes mellitus, age, irregular supportiveperiodontal therapy and ineffective plaque control)have been shown to increase the risk for tooth lossduring supportive periodontal therapy in patientswith chronic periodontitis (13–15, 48, 59). A higherrisk for disease recurrence and tooth loss after activeperiodontal therapy can be anticipated in patientswith aggressive periodontitis than in patients withchronic periodontitis because of a higher susceptibil-ity for disease progression in patients in the formergroup. However, the risk factors for tooth loss and/orrecurrence of periodontitis in patients with aggressiveperiodontitis have only recently been investigated.Few studies have assessed the mean tooth loss inpatients with aggressive periodontitis during support-ive periodontal therapy (8, 35, 85). The mean annualtooth loss for these patients seems to range from 0.11(85) to 0.29 (35) teeth, although in the latter studyalso untreated patients were included. In the recentretrospective study of Baumer et al. (8), tooth loss of0.13 teeth/year was calculated in patients withaggressive periodontitis. Interestingly, when theauthors differentiated between the different types ofaggressive periodontitis, patients with generalizedaggressive periodontitis exhibited a higher tooth loss,of 0.14 teeth/year, whereas patients with localizedaggressive periodontitis only lost 0.02 teeth/year. Anadditional analysis showed that patients with aggres-sive periodontitis who followed the supportive peri-odontal care regularly had a tooth loss of 0.075 teeth/year, whereas patients with irregular periodontal carehad a tooth loss of 0.15 teeth/year, stressing theimportance of regular periodontal supportive ther-apy. Age, low educational status and absence of theinterleukin-1 composite genotype were significantlycorrelated with tooth loss and could be defined as riskfactors. Nearly significant correlations could be foundfor smoking, type of aggressive periodontitis, irregularsupportive periodontal therapy and the plaque-con-trol record. In terms of risk factors for disease recur-rence (defined as the occurrence of probing pocketdepths of 5 mm or more at 30% or more of the teeth),Baumer et al. (8) also identified smoking as the mainsignificant risk factor, thereby confirming the datafrom Kamma & Baehni (40). In the latter study, theauthors also identified stress as a significant predic-tive factor for future clinical attachment loss. Thetype of aggressive periodontitis was a nearly signifi-cant risk factor for which patients with generalized
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aggressive periodontitis showed an odds ratio of 35.2for recurrence and which confirms the results of stud-ies showing long-term stability of the disease inpatients with localized aggressive periodontitis (35,65). Additionally, an elevated gingival bleeding indexand a high plaque-control record showed odds ratiosof 31.1 and 63.8, respectively, for disease recurrence.No statistical analysis could be performed for sup-portive periodontal treatment as a risk factor fordisease recurrence because none of the patientsreceiving regular supportive periodontal therapyexperienced recurrence of the disease. However, thisstresses the effectiveness of this risk factor. In sum-mary, age, educational status, generalized aggressiveperiodontitis (vs. localized aggressive periodontitis),absence of the interleukin-1 composite genotype,irregular supportive periodontal therapy, smoking,high mean gingival bleeding index and high plaque-control records are important risk factors for diseaserecurrence or tooth loss in patients with aggressiveperiodontitis. Of these, maintenance of supportiveperiodontal therapy, smoking, high mean gingivalbleeding index and high plaque-control records aremodifiable risk factors, and the latter two are corre-lated with the patient’s oral hygiene. Therefore, itseems tempting to support the daily oral hygiene ofaggressive periodontitis patients with antiseptics aspart of the supportive periodontal therapy. To date,only one trial, performed by Guarnelli et al. (32) in 18patients, has evaluated the effect of an amine fluo-ride/stannous fluoride-containing mouthrinse inpatients with aggressive periodontitis. In a cross-over clinical trial this mouthrinse was effective forreducing the amount of supragingival plaque depos-its. However, there was no significant difference com-pared with the placebo mouthwash on the gingivitisindex. The impact of these results on disease progres-sion and tooth loss has not been determined.
Regular supportive periodontal therapy has beenshown to be effective in controlling the progressionof aggressive periodontitis. Maintenance therapy isconsidered to be a lifelong requirement, but the fre-quency of recall visits is unclear. The use of manydifferent protocols is being reported in the litera-ture. Deas & Mealey (23) stated that monthly intervalsare advisable during the first 6 months of mainte-nance. Some studies have reported an effective con-trol of disease progression using three to four recallvisits per year. To date there are no studies compar-ing the effect of different follow-up intervals inpatients with aggressive periodontitis. In order todefine such intervals for patients with chronic peri-odontitis, the periodontal risk assessment, which
estimates the patient’s risk profile for the progressionof periodontitis, based on six risk factors, was created(47). Meyer-Baumer et al. (63) recently attempted toconfirm the prognostic value of the model inaggressive periodontitis. When the interleukin-1composite genotype was not taken into account, theimpact of this model could be shown to be statisti-cally significant and allowed patients with aggressiveperiodontitis to be characterized into different riskgroups.
Finally, needless to say, each visit for supportiveperiodontal treatment should consist of a thoroughmedical review, an inquiry into recent periodontalproblems, an extensive oral examination, a renewal oforal-hygiene instructions, debridement of residualpockets and prophylaxis. Also, the need to controlmodifiable risk factors, such as smoking, must bestressed to the patient.
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