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Antibiotics in Periodontics: Right or Wrong?

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It is well established that periodontal infections are caused by bacterial deposits in supra- and subgingival dental plaque. These infections respond well to measures that aim to reduce the periodontal bacterial load, and clinical improvement occurs when the bacterial challenge is compatible with the host’s immunocompetence. It has also been established that systemic antibiotics can significantly enhance the effects of mechanical periodontal therapy, i.e., scaling and root planing in conjunction with measures that improve the oral hygiene level. 1-3 A minor proportion of the patients with periodontitis does not respond adequately to mechanical treatment, and factors such as smoking, stress, reduced immunocompetence and systemic diseases are held responsible. 3 These patients are prime candidates for adjunctive systemic antimicrobial therapy. A combination of metronidazole and amoxicillin (MA) has shown to be an effective antibiotic regime to combat Aggregatibacter actinomycetemcomitans- (previously Actinobacillus actinomycetemcomitans) and Porphyromonas gingivalis-associated periodontal infections. 4-6 Recently, Cionca et al. 7 reported on the adjunctive use of this antibiotic regimen in conjunction to full-mouth scaling and root planing in patients with moderate to severe chronic periodontitis. Guerreo et al. 6 used a comparable treatment protocol in patients with aggressive periodontitis and showed significantly better improvement of all periodontal parameters in the antibiotic-treated patients compared to placebo-treated subjects 6 months post-treatment. In both clinical trials, the so-called full-mouth disinfection approach was used. This implies scaling and root planing of all affected teeth within 48 hours, subgingival irrigation with chlorhexidine, and chlorhexidine rinsing for 14 days after subgingival treatment. This approach is based on the assumption that untreated periodontal sites may be the source of infection of already treated lesions. This hypothesis of intraoral reinfection has never been proven and cannot be proven based on a clinical protocol. Moreover, it is very unlikely that mechanical periodontal treatment results in complete subgingival elimination of key periodontal path
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Commentary
Antibiotics in Periodontics: Right or Wrong?
Arie J. van Winkelhoff* and Edwin G. Winkel*
It is well established that periodontal infections are
caused by bacterial deposits in supra- and sub-
gingival dental plaque. These infections respond
well to measures that aim to reduce the periodontal
bacterial load, and clinical improvement occurs
when the bacterial challenge is compatible with the
host’s immunocompetence. It has also been estab-
lished that systemic antibiotics can significantly
enhance the effects of mechanical periodontal ther-
apy, i.e., scaling and root planing in conjunction with
measures that improve the oral hygiene level.
1-3
A
minor proportion of the patients with periodontitis
does not respond adequately to mechanical treat-
ment, and factors such as smoking, stress, reduced
immunocompetence and systemic diseases are held
responsible.
3
These patients are prime candidates for
adjunctive systemic antimicrobial therapy. A com-
bination of metronidazole and amoxicillin (MA) has
shown to be an effective antibiotic regime to combat
Aggregatibacter actinomycetemcomitans- (previ-
ously Actinobacillus actinomycetemcomitans) and
Porphyromonas gingivalis-associated periodontal
infections.
4-6
Recently, Cionca et al.
7
reported on
the adjunctive use of this antibiotic regimen in
conjunction to full-mouth scaling and root planing in
patients with moderate to severe chronic periodon-
titis. Guerreo et al.
6
used a comparable treatment
protocol in patients with aggressive periodontitis and
showed significantly better improvement of all peri-
odontal parameters in the antibiotic-treated patients
compared to placebo-treated subjects 6 months
post-treatment. In both clinical trials, the so-called
full-mouth disinfection approach was used. This
implies scaling and root planing of all affected teeth
within 48 hours, subgingival irrigation with chlorhex-
idine, and chlorhexidine rinsing for 14 days after
subgingival treatment. This approach is based on the
assumption that untreated periodontal sites may be
the source of infection of already treated lesions.
This hypothesis of intraoral reinfection has never
been proven and cannot be proven based on a
clinical protocol. Moreover, it is very unlikely that
mechanical periodontal treatment results in com-
plete subgingival elimination of key periodontal path-
ogens such as P. gingivalis,Tannerella forsythia
(previously T. forsythensis), or A. actinomycetemco-
mitans at treated sites.
8,9
This notion makes the
discussion of intraoral reinfection rather superfluous.
In most other studies on MA,
2
the quadrant-wise
approach of non-surgical treatment was used. In a
meta-analysis, it was shown that conventional quad-
rant scaling and root planing is equally effective as the
48-hour protocol.
10
Therefore, the beneficial clinical
effects in the Guerrero et al.
6
and Cionca et al.
7
studies can be attributed to the use of adjunctive MA
therapy.
The use of adjunctive MA has been studied in
double-masked, placebo-controlled clinical trials,
5-7
and these studies have revealed that, inchronic as well
as in aggressive periodontitis, the antibiotics result in
better resolution of the periodontal inflammation, bet-
ter probing depths (PDs), and attachment loss reduc-
tion. All three studies clearly showed that the number
of pockets 5 mm was better reduced with antibiotics
compared to placebo medication. For instance, Guerrero
et al.
6
showed that, 6 months after active treatment,
the number of sites changing from 5to£4 mm was
significantly higher in the antibiotic-treated patients
than in the placebo-treated subjects (74% versus
54%; P=0.008) as were the pockets that changed
from 4to£3 mm (55% versus 37%; P=0.038). These
observations show that the number of teeth that
needed further treatment was significantly reduced
by adjunctive antibiotic therapy (Table 1). This phe-
nomenon is not new and has been reported after the
use of systemic metronidazole.
11
Cionca et al.
7
calculated the protective risk for fur-
ther periodontal therapy, defined as more than one
site with PD 5 mm post-treatment. Backward, step-
wise logistic regression analysis revealed that, at 6
months, only the use of antibiotics (P=0.01) but
not plaque score, gender, or smoking, determined
the need for further periodontal treatment. The protec-
tive risk amounted to 8.85. The protective risk of an-
tibiotic use for more than one site with PD 5mm6
months after treatment amounted to 15.62 (P=0.01).
This means that a subject using systemic MA as
an adjunct to mechanical periodontal treatment was
* Department of Dentistry and Oral Hygiene, University Medical Center
Groningen, Groningen, The Netherlands. doi: 10.1902/jop.2009.090276
J Periodontol October 2009
1555
protected by a factor of 15.62 from further periodontal
treatment.
ANTIBIOTICS FOR ALL?
Should we treat all patients with destructive peri-
odontal diseases with antibiotics? Haffajee,
12
in her
response to van Winkelhoff,
13
summarized some rel-
evant questions in relation to the administration of an-
tibiotics in the treatment of periodontitis. One critical
issue is the concern over which patients would benefit
most from systemic antibiotic administration.
The study of Cionca et al.
7
does not provide an an-
swer to this particular concern, although Figures 2
and 3 in their article clearly indicate a number of out-
liners. They selected their patients on clinical criteria
only. It is well documented that periodontitis is asso-
ciated with different clusters of specific subgingival
bacterial species.
14,15
Therefore, it is questionable
whether one single antibiotic regimen will be equally
effective in all periodontitis patients. Therefore, the
statement of the authors
7
that ‘‘the use of systemic an-
tibiotics should not be restricted to specific groups of
periodontal patients, for example those with highly
active diseases or a specific microbiological profile’’
is not based on the authors’ observations. They have
not analyzed the clinical results in relations to baseline
microbiologic data. However, do we have data to indi-
cate that not all patients respond equally well to
MA therapy? Yes, we do. In a randomized, double-
masked, placebo-controlled study, Winkel et al.
5
showed that the significantly better improvement in
full-mouth PD reduction in patients that used MA was
mainly produced by patients positive for P. gingivalis
at baseline (Fig. 1). In addition, the significantly greater
reduction of sites no longer needing additional treat-
ment (i.e., sites with PD <5 mm) after scaling and root
planing plus antibiotics was produced by patients who
were positive for P. gingivalis at baseline (Fig. 2).
Equally important was the notion that subjects without
detectable P. gingivalis at baseline responded equally
well to placebo and test medication in terms of PD re-
duction and reduction of the number of sites 5 mm. In
other words, the subgingival microbial profile at base-
line may be one determining factor of the clinical ef-
fects of systemic antimicrobial therapy. Therefore,
treatment of P. gingivalis-negative patients with anti-
biotics may be considered overtreatment.
Are They all Equal?
A second issue raised by Haffajee
12
was the concern
whether all antibiotics are equally effective. The clin-
ical trials in which different systemically administered
antibiotics were studied clearly indicate that this is
not the case. Haffajee et al.
16
showed clinical superi-
ority of metronidazole over azithromycin. Better clin-
ical outcome with metronidazole and clindamycin
than tetracycline has also been reported in severe
aggressive periodontitis.
17
In a double-masked,
Table 1.
Percentage of Sites That Changed From
PD 5to<5 mm and That Had Clinical
Attachment Gain (CAG) 2 mm in Patients
Treated With Placebo (P) or MA (test)
Treatment
PD 5to
<5mm CAG2 mm Evaluation Study
P 24.3* 20.2* 3 months Winkel et al.
5
Test 31.8 25.1
P 54.2* 16.1* 6 months Guerrero et al.
6
Test 74.1 25.4
* Significantly different (P<0.05) between P and test medication.
Metronidazole (250 mg) plus amoxicillin (375 mg); both drugs 3 times a
day for 7 days.
Metronidazole (500 mg) plus amoxicillin (500 mg); both drugs 3 times a
day for 7 days.
Figure 1.
Full-mouth PD change after scaling and root planing and placebo (P)
or MA (test [T]) therapy in patients with (+) or without (-)
P. gingivalis (Pg) at baseline. Based on data from Winkel et al.
5
Figure 2.
Mean reduction of sites (%) with PD 5 mm after scaling and root
planing in subjects with (+)orwithout(-)P. gingivalis (Pg) at baseline
treated with placebo (P) or MA (test [T]). Based on data from Winkel
et al.
5
Antibiotics in Periodontics Volume 80 • Number 10
1556
placebo-controlled clinical trial,
18
it was shown that
protected amoxicillin did not improve the clinical out-
come to a measurable extent over a period of 12
months, nor did the antibiotic therapy perform better
in suppressing key periodontal pathogens. In none of
these studies were patients selected on the basis of
subgingival microbiologic profile. Clearly, some anti-
biotics in periodontics are more equal than others.
Maybe Not?
What is the down side of antibiotic administration?
The use of antibiotics has also introduced the
emergence of bacterial resistance to one or multiple
antibiotics. This worldwide problem can not be under-
estimated. It is mainly caused by abuse, misuse, and
poor compliance to the medication. The use of antibi-
otics is associated with adverse effects in a significant
number of subjects.
6-8
These range from minor and
transient complaints such as nausea, headache, and
altered taste to pseudomembranous colitis. In addi-
tion, antibiotics can cause interactions with other
medications.
CONCLUSIONS
The systemic use of antibiotics in the treatment of se-
vere periodontitis has proven to be clinically advanta-
geous. There is strong evidence that not all antibiotics
are equally effective. So far, MA therapy seems to
have the best clinical outcome.
2
It is not clear whether
all patients will equally benefit from antibiotics. There
is an indication that the baseline microbial profile de-
termines the outcome of antibiotic-based periodontal
treatment.
5
We know that periodontitis is not a spe-
cific bacterial disease but a compilation of different
bacterial disorders. This observation should become
part of our thinking when designing new studies with
antibiotics in periodontics. We do not need more stud-
ies without a sound microbiologic analysis in relation
to the clinical outcome parameters. The outcome of
these studies should assist clinicians in future deci-
sion-making: as to whether or not to prescribe antibi-
otics and if so, during which stage of periodontal
treatment.
Before we prescribe antibiotics to all periodontitis
patients, we need to find out which bacterial profile re-
sponds best to which antibiotic. If it is true that subjects
without P. gingivalis do not benefit from adjunct MA,
then we need to stop prescribing these potent drugs
for this form of periodontitis. Then, we need to find
out whether or not these subjects respond to an alter-
native antibiotic regimen. Antibiotics for all? No, not
yet.
ACKNOWLEDGMENT
The authors report no conflicts of interest related to
this commentary.
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Correspondence: Dr. Arie J. van Winkelhoff, Department
of Dentistry and Oral Hygiene, University Medical Center
Groningen, Antonius Deusinglaan 1, 9713 AV Groningen,
The Netherlands. E-mail: a.j.van.winkelhoff@med.
umcg.nl.
Submitted May 15, 2009; accepted for publication May 15,
2009.
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... The use of antibiotics in periodontics remains a very controversial topic. The trends have been evolving and the subject remains on top of current topics, notably with the emergence of bacterial resistances (64,65). Moreover, every country has a different approach regarding antibiotics use and even the ESE (European Society of Endodontics) for example states its position about their uses but claims that local recommendations may differ (66). ...
Thesis
Les maladies parodontales, de prévalence élevée, sont largement répandues à travers les populations humaines. Leurs conséquences sont multiples, altérant fortement la qualité de vie comme la santé globale et ont un impact économique important. Elles sont la conséquence d’une infection bactérienne à laquelle est associée une réponse inflammatoire inadéquate. Ces mécanismes entrainent la destruction des tissus de soutien de la dent (gencive, ligament, os alvéolaire) menant à la perte dentaire. De plus, il est prouvé que le statut parodontal est associé à de nombreuses autres pathologies et on estime que la parodontite aggrave certaines autres pathologies comme le diabète par exemple. Le traitement de référence consiste en l’élimination mécanique de la plaque dentaire sous-gingivale, opération appelée surfaçage radiculaire. En pratique, ce geste est souvent accompagné de la prise d’antibiotiques par voie systémique, engendrant de nombreux effets indésirables et dont l’efficacité reste à améliorer. Ainsi, la nécessité d’améliorer la prise en charge de la maladie peut être comblée par le développement de systèmes à libération locale de substances actives. L’objectif de ce travail consiste à développer et caractériser physico chimiquement un implant se formant in-situ (ISFI). Ce système très spécifique est une formulation liquide destinée à former un implant solide après injection dans la poche parodontale, libérant deux substances actives de manière contrôlée. Afin d’éviter l’augmentation des résistances bactériennes vis-à-vis des antibiotiques, ce dispositif est formulé avec des antiseptiques (ex. chlorhexidine). Ensuite, afin de favoriser la cicatrisation parodontale, un agent anti-inflammatoire est également utilisé (ex. ibuprofène). Ce travail décrit dans un premier temps l’état des lieux sur ce type de dispositif et en particulier les implants se formant in-situ. Ensuite, la section expérimentale décrit la formulation des implants et les méthodes utilisées pour les caractériser. Les effets des paramètres de formulation sur les propriétés physico-chimiques des systèmes et en particulier les cinétiques de libération sont discutées au regard des besoins de la pratique clinique pour ce type de dispositif.
... Data from the United States show that up to 60% of the microorganisms isolated from infected surgical wounds was antibiotic resistant [65]. Concerns have also been raised that an extensive use of systemic antibiotics in periodontal therapy, particularly when administered to counterbalance incomplete mechanical instrumentation or poor oral hygiene, could contribute substantially to the development of bacterial antimicrobial resistance [72][73][74]. Similar concerns should be expressed to periimplantitis treatment protocol comprising systemically Table 4 Included and excluded primary studies ...
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Background Microbial biofilm accumulation is the main cause of peri-implantitis. The majority of surgical peri-implantitis treatment protocols suggests adjunctive use of systemic antibiotics to target specific putative bacteria. The aim of this systematic review was to critically evaluate the adjunctive use of systemically administered antibiotics in surgical treatment of peri-implantitis by reviewing previously published systematic reviews and primary studies. Methods A systematic literature search was conducted in four electronic databases (MEDLINE, The Cochrane Library, EMBASE, and Web of Science) for randomised controlled trials, cohort studies, case–control studies, and systematic reviews reporting surgical treatment of peri-implantitis with and without adjunctive systemically administered antibiotic therapy. The included systematic reviews and primary studies were qualitatively assessed using AMSTAR and GRADE, respectively. No restrictions were set for date of publication, journal, or language. Results The literature search identified 681 papers. Only seven systematic reviews and two primary studies met the inclusion criteria. Four out of seven included systematic reviews concluded that no evidence exists for use of systemic antibiotics to improve the clinical outcomes in surgical treatment of peri-implantitis. One review did not estimate the level of evidence, one did not clearly state any beneficial effect, whereas one reported a limited adjunctive effect. Further, the two included primary studies did not show a long-term significant benefit of adjunctive use of systemically administrated antibiotics. However, one study reported a short-term adjunctive effect in patients with modified surface implants. Due to heterogeneity in study design, low number of included primary studies, and grade of bias, no meta-analysis was performed. Conclusion The use of systemically administered antibiotics as an adjunct to surgical interventions of peri-implantitis cannot be justified as a part of a standard treatment protocol. A pervasive problem is the lack of uniform diagnosis criteria for peri-implantitis, deficient information about patient characteristics, absence of high quality long-term randomised controlled trials, and authors’ declaration on conflict of interest.
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It has been suggested that scaling and root planing of all pockets within a few hours and chlorhexidine treatments (full-mouth disinfection) may reduce the need for supplementary therapies. The aim of this study was to evaluate the clinical benefit of amoxicillin and metronidazole administered immediately after completion of full-mouth periodontal debridement in patients with chronic periodontitis. This was a single-center, double-masked, placebo-controlled, randomized longitudinal study of 6 months' duration. Fifty-one patients received full-mouth periodontal debridement, performed within 48 hours. Twenty-five subjects received metronidazole, 500 mg, and amoxicillin, 375 mg, three times a day for 7 days; 26 subjects received a placebo. Forty-seven patients could be followed up to month 6. No differences in clinical parameters were noted before treatment. The overall mean probing depth decreased from 4.3 +/- 0.4 mm to 3.0 +/- 0.2 mm in the test group and from 4.4 +/- 0.4 mm to 3.1 +/- 0.3 mm in the control group (P = 0.05, difference between groups). More importantly, test subjects had a significantly lower mean number of persisting pockets >4 mm and bleeding on probing that required further treatment (P = 0.005): 6 months after full-mouth debridement plus antibiotics, only 0.4 +/- 0.8 persisting pockets were still present, whereas 3.0 +/- 4.3 persisting pockets were still present in the control group. The protective risk of the antibiotics for having more than one pocket deeper than 4 mm and bleeding on probing per subject after 6 months was 8.85. Systemic metronidazole and amoxicillin significantly improved the 6-month clinical outcomes of full-mouth non-surgical periodontal debridement, thus significantly reducing the need for additional therapy.
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It has been recognized for some time that bacterial species exist in complexes in subgingival plaque. The purpose of the present investigation was to attempt to define such communities using data from large numbers of plaque samples and different clustering and ordination techniques. Subgingival plaque samples were taken from the mesial aspect of each tooth in 185 subjects (mean age 51 +/- 16 years) with (n = 160) or without (n = 25) periodontitis. The presence and levels of 40 subgingival taxa were determined in 13,261 plaque samples using whole genomic DNA probes and checkerboard DNA-DNA hybridization. Clinical assessments were made at 6 sites per tooth at each visit. Similarities between pairs of species were computed using phi coefficients and species clustered using an averaged unweighted linkage sort. Community ordination was performed using principal components analysis and correspondence analysis. 5 major complexes were consistently observed using any of the analytical methods. One complex consisted of the tightly related group: Bacteroides forsythus, Porphyromonas gingivalis and Treponema denticola. The 2nd complex consisted of a tightly related core group including members of the Fusobacterium nucleatum/periodonticum subspecies, Prevotella intermedia, Prevotella nigrescens and Peptostreptococcus micros. Species associated with this group included: Eubacterium nodatum, Campylobacter rectus, Campylobacter showae, Streptococcus constellatus and Campylobacter gracilis. The 3rd complex consisted of Streptococcus sanguis, S. oralis, S. mitis, S. gordonii and S. intermedius. The 4th complex was comprised of 3 Capnocytophaga species, Campylobacter concisus, Eikenella corrodens and Actinobacillus actinomycetemcomitans serotype a. The 5th complex consisted of Veillonella parvula and Actinomyces odontolyticus. A. actinomycetemcomitans serotype b, Selenomonas noxia and Actinomyces naeslundii genospecies 2 (A. viscosus) were outliers with little relation to each other and the 5 major complexes. The 1st complex related strikingly to clinical measures of periodontal disease particularly pocket depth and bleeding on probing.
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Systemic antibiotics in conjunction with scaling and root planing (SRP), can offer an additional benefit over SRP alone in the treatment of periodontitis, in terms of clinical attachment loss (CAL) and pocket depth change, and reduced risk of additional CAL loss. However, antibiotics are not innocuous drugs. Their use should be justified on the basis of a clearly established need and should not be substituted for adequate local treatment. The aim of this review is to discuss the rationale, proper selection, dosage and duration for antibiotic therapy so as to optimize the usefulness of drug therapy.
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Background: In an attempt to enhance treatment outcomes, alternative protocols for anti-infective periodontal therapy have been introduced. Objectives: To evaluate the effectiveness of full-mouth disinfection or full-mouth scaling compared to conventional quadrant scaling for periodontitis. Search strategy: Data sources included electronic databases, handsearched journals and contact with experts. The Cochrane Oral Health Group Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and EMBASE were searched. Reference lists from relevant articles were scanned and the authors of eligible studies were contacted to identify trials and obtain additional information. Date of most recent searches: December 2006: (CENTRAL) (The Cochrane Library 2006, Issue 4). Selection criteria: Randomised controlled trials were selected with at least 3 months follow up comparing full-mouth scaling and root planing within 24 hours with (FMD) or without (FMS) the adjunctive use of an antiseptic (chlorhexidine) with conventional quadrant scaling and root planing (control). The methodological quality of the studies was assessed within the data extraction form, mainly focusing on: method of randomisation, allocation concealment, blindness of examiners and completeness of follow up. Data collection and analysis: Data extraction and quality assessment were conducted independently by multiple review authors. The primary outcome measure was tooth loss, secondary outcomes were reduction of probing depth, bleeding on probing and gain in probing attachment. The Cochrane Collaboration statistical guidelines were followed. Main results: The search identified 216 abstracts. Review of these abstracts resulted in 12 publications for detailed review. Finally, seven randomised controlled trials (RCTs) which met the criteria for eligibility were independently selected by two review authors. None of the studies included reported on tooth loss. All treatment modalities led to significant improvements in clinical parameters after a follow up of at least 3 months. For the secondary outcome, reduction in probing depth, the mean difference between FMD and control was 0.53 mm (95% confidence interval (CI) 0.28 to 0.77) in moderately deep pockets of single rooted teeth and for gain in probing attachment 0.33 mm (95% CI 0.04 to 0.63) in moderately deep single and multirooted teeth. Comparing FMD and FMS the mean difference in one study for gain in probing attachment amounted to 0.74 mm in favour of FMS (95% CI 0.17 to 1.31) for deep pockets in multirooted teeth, while another study reported a mean difference for reduction in bleeding on probing of 18% in favour of FMD (95% CI -34.30 to -1.70) for deep pockets of single rooted teeth. No significant differences were observed for any of the outcome measures, when comparing FMS and control. Authors' conclusions: In patients with chronic periodontitis in moderately deep pockets slightly more favourable outcomes for pocket reduction and gain in probing attachment were found following FMD compared to control. However, these additional improvements were only modest and there was only a very limited number of studies available for comparison, thus limiting general conclusions about the clinical benefit of full-mouth disinfection. Copyright © 2008 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.
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Thesis (doctoral)--Universiteit van Amsterdam, 2000. Includes bibliographical references.
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We report on the microbiological and clinical effects of mechanical debridement in combination with metronidazole plus amoxicillin therapy in 118 patients with Actinobacillus actinomycetemcomitans-associated periodontitis. Patients were categorized into 3 groups: 28 had localized periodontitis; 50 had generalized periodontitis, and 40 had refractory periodontitis. After initial treatment and metronidazole plus amoxicillin therapy 114 of 118 (96.6%) patients had no detectable A. actinomycetemcomitans. Significant reduction in pocket probing depth and gain of clinical attachment were achieved in almost all patients. Four patients were still positive for A. actinomycetemcomitans after therapy. Metronidazole resistance (MIC greater than 25 micrograms/ml) was observed in 2 of 4 strains from these patients. Patients still positive for A. actinomycetemcomitans or Porphyromonas gingivalis showed a significant higher bleeding tendency after therapy. It was concluded that mechanical periodontal treatment in combination with the metronidazole plus amoxicillin therapy is effective for subgingival suppression of A. actinomycetemcomitans in patients with severe periodontitis.
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A considerable amount of circumstantial evidence indicates that most forms of periodontitis are due to the presence or dominance of a finite number of bacterial species in the subgingival plaque. Almost all of the putative pathogens are anaerobic species, indicating that most forms of periodontitis could be diagnosed as anaerobic infections. In this double-blind investigation, patients with elevated proportions or levels of spirochetes in 2 or more plaque samples, i.e., 60% spirochetes, were randomly assigned to receive either metronidazole, 250 mg 3 x a day for 1 week, or placebo (positive-control) after the completion of all debridement procedures. When the patients were re-examined 4 to 6 weeks later, the patients in the metronidazole group (n = 15) exhibited a highly significant (p less than 0.01) reduction in probing depth and apparent gain in attachment levels relative to the patients (n = 18) in the positive-control group about those teeth that initially had probing depths of 4 to 6 mm. This pattern was also observed about teeth that initially had probing depths greater than or equal to 7 mm. This reduction in probing depths and apparent gain in attachment was associated with a significant reduction in the need for periodontal surgery in the metronidazole-treated patients (difference 8.4 teeth per patient) compared to the positive-control patients (2.6 teeth per patient). These clinical improvements in the metronidazole group were associated with significantly lower proportions of spirochetes, selenomonads, motile rods, and P. intermedius, and a significantly higher proportion of cocci in the plaques. These findings indicate that systemic metronidazole, when given after all the root surface debridement is completed, leads to additional treatment benefits, including a reduced need for surgery, beyond that which can be achieved by debridement alone.
Article
It has been recognized for some time that bacterial species exist in complexes in subgingival plaque. The purpose of the present investigation was to attempt to define such communities using data from large numbers of plaque samples and different clustering and ordination techniques. Subgingival plaque samples were taken from the mesial aspect of each tooth in 185 subjects (mean age 51 +/- 16 years) with (n = 160) or without (n = 25) periodontitis. The presence and levels of 40 subgingival taxa were determined in 13,261 plaque samples using whole genomic DNA probes and checkerboard DNA-DNA hybridization. Clinical assessments were made at 6 sites per tooth at each visit. Similarities between pairs of species were computed using phi coefficients and species clustered using an averaged unweighted linkage sort. Community ordination was performed using principal components analysis and correspondence analysis. 5 major complexes were consistently observed using any of the analytical methods. One complex consisted of the tightly related group: Bacteroides forsythus, Porphyromonas gingivalis and Treponema denticola. The 2nd complex consisted of a tightly related core group including members of the Fusobacterium nucleatum/periodonticum subspecies, Prevotella intermedia, Prevotella nigrescens and Peptostreptococcus micros. Species associated with this group included: Eubacterium nodatum, Campylobacter rectus, Campylobacter showae, Streptococcus constellatus and Campylobacter gracilis. The 3rd complex consisted of Streptococcus sanguis, S. oralis, S. mitis, S. gordonii and S. intermedius. The 4th complex was comprised of 3 Capnocytophaga species, Campylobacter concisus, Eikenella corrodens and Actinobacillus actinomycetemcomitans serotype a. The 5th complex consisted of Veillonella parvula and Actinomyces odontolyticus. A. actinomycetemcomitans serotype b, Selenomonas noxia and Actinomyces naeslundii genospecies 2 (A. viscosus) were outliers with little relation to each other and the 5 major complexes. The 1st complex related strikingly to clinical measures of periodontal disease particularly pocket depth and bleeding on probing.
Article
1. Periodontal disease may result from endogenous infections (F. nucleatum in gingivitis), opportunistic infections (P. intermedia in insulin-dependent diabetes periodontitis), superinfections (Candida, enteric rods and Pseudomonas in adult periodontitis) and true infections (A. actinomycetemcomitans and P. gingivalis in advanced adult periodontitis). 2. Periodontal treatment aims at restoring a microbiota compatible with periodontal health. Effective therapy implies a reduction of pathogenic levels of indigenous oral microorganisms and an elimination of exogenous pathogens and of organisms outside their ecological niche such as enteric rods and pseudomonads. Since both microbial and host susceptibility factors determine the periodontal health status, the composition and number of subgingival organisms associated with periodontal health may vary from individual to individual. 3. Mechanical periodontal treatment can reduce total supra- and subgingival bacterial mass, but major pathogens may escape the effect of treatment due to their ability to invade periodontal tissues or to reside in furcations or other tooth structures outside the reach of periodontal instruments, or due to poor host defense mechanisms. 4. Systemic periodontal antibiotic therapy aims to reinforce mechanical periodontal treatment and to support the host defense system in overcoming the infection by killing subgingival pathogens that remain after conventional mechanical periodontal therapy. 5. Single antimicrobial drug therapies are able to suppress the number of subgingival indigenous bacteria for a prolonged period of time depending on the host defense and oral hygiene efforts. Combination drug therapies aim at enlarging the antimicrobial spectrum and exploiting synergy between antibiotics and may be indicated with complex mixed subgingival infections. Much has been learned about the microbiological etiology of destructive periodontal disease and the effectiveness of various periodontal therapies. Successful periodontal treatment depends on proper assessment of an individual's risk for periodontal breakdown which, in turn, depends on the pathogenic characteristics of the periodontal microbiota and the host susceptibility. Therapeutic success in periodontal therapy will undoubtedly increase with improved ability to diagnose the periodontal infection and critical host factors and to apply individually tailored periodontal treatments using an armamentarium of locally and systemically applied therapeutic agents.
Article
The aims of this study were to evaluate the clinical and microbiological effects of initial periodontal therapy (IT) and to determine the additional effects of systemic amoxicillin (Flemoxin Solutab) 375 mg TID plus metronidazole 250 mg TID therapy, in patients with adult Actinobacillus actinomycetemcomitans (Aa)-associated periodontitis in conjunction with either Porphyromonas gingivalis (Pg), Bacteroides forsythus (Bf) and/or Prevotella intermedia (Pi). In addition the adverse effects of the antimicrobial therapy were also documented. A total of 22 patients were enrolled. The deepest, bleeding pocket in each quadrant was selected and at these 4 experimental sites clinical measurements and microbiological testing was carried out at baseline, after (IT), i.e., 21 weeks after baseline, and after antimicrobial therapy (AM), i.e., 35 weeks after baseline. At baseline, the mean plaque index (PI) amounted 0.5, 0.1 after IT and 0.3 after systemic AM. The mean bleeding index decreased from 1.6 to 1.2 after IT and a further decrease to 0.7 after AM was noted. Suppuration was completely eliminated after AM. The mean change of probing pocket depth (PPD) after IT amounted 1.4 mm and was further reduced with an additional mean change of 1.1 mm after medication. Clinical attachment gain was 1.1 mm after IT and an additional 0.9 mm was observed after AM. One of the 22 Aa positive patients and 4 of 17 Pg positive patients became negative for these species after IT. The number of patients with detectable Pi decreased from 16 to 10 after IT. After AM, in comparison to baseline, suppression below detection level for Aa was achieved in 19 out of 22, for Pg in 9 out of 17, for Bf in 13 out of 14, and for Pi in 11 out of 16 patients. By contrast, higher frequencies of Peptostreptococcus micros and Fusobacterium nucleatum were found after AM. On the basis of the microbiological results the study group was separated into 2 subgroups: group A consisted of subjects who had no detectable levels of Aa, Pg, Bf and <5% of Pi after AM. Group B consisted of those who still showed presence of one of these 3 species and/or > or =5% levels of Pi. After AM, group B had significantly higher PI, BI, PPD and CAL scores then group A. It is concluded that group A showed low plaque scores and no detectable periodontal pathogens. This microbiological condition has been associated with a long-term stable periodontium.