Aggressive Periodontitis - Guidelines for Diagnosis and Management of

Publication: 23/02/2017  --
Last review: 01/01/1900  
Next review: 01/02/2020  
Clinical Guideline
ID: 4917 
Approved By: Improving Antimicrobial Prescribing Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2017  


This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Guidelines for Diagnosis and Management of Aggressive Periodontitis

  • Treatment Algorithm
  • Summary
    Aggressive Periodontitis

    Pertinent aspects of history and examination
    Key diagnostic criteria

    Investigations required

    • Microbiology, Haematology, Clinical Chemistry, Immunology etc.
    • Radiology
    • Other

    Non-Antimicrobial Management
    e.g. fluid, steroids etc

    Empirical (initial) antimicrobial treatment include- specify antimicrobial agent(s), dose, route of administration, antimicrobial allergy, duration of treatment, switch to oral agent(s)

    Referral criteria for specialist input

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    Periodontitis is a condition that involves the progressive destruction of the supporting tissues of the teeth in response to oral microorganisms in plaque.1 This may ultimately result in tooth loss. Aggressive periodontitis (AgP) is a relatively rare subset of this condition with strong familial and racial aggregations. It has an estimated prevalence of 0.1% in Caucasian populations and between 1% and 5% in Afro-Caribbean populations, but there are inconsistencies in case definitions.2  AgP can be defined by the primary and secondary features described by Armitage in 19991:

    Primary features:

    1.  Familial aggregation
    2.  Rapid attachment loss and bone destruction
    3.  Systemically well

    Secondary (laboratory) features (often present):

    1.  Amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction;
    2.  Elevated proportions of A. Actinomycetemcomitans and, in some populations, P. gingivalis;
    3.  Phagocyte abnormalities;
    4.  Progression of attachment loss and bone loss may be self-arresting;
    5.  Hyper-responsive macrophage phenotype, including elevated levels of prostaglandin E2 (PGE2) and interleukin-1β (IL-1 )

    The condition can be categorised as localised or generalised. Localised AgP tends to affect specific teeth (normally the first molars and incisors) whereas other teeth are periodontally healthy and unaffected. Generalised AgP is defined as affecting three or more permanent teeth apart from the first molars and incisors. In this case, patients typically have a poor serum antibody response and the disease course may be episodic in nature.

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    Clinical Diagnosis

    As many clinical signs and symptoms of aggressive periodontitis are common to all sub-classifications of periodontitis, arriving at a diagnosis relies on the combination of information gained during history taking and clinical examination. The key information that may differentiate a case of aggressive periodontitis is related to the amount and pattern of periodontal destruction and the patient's age and medical status.3 A patient who is young, medically healthy and presents with advanced periodontal destruction is likely to have a form of aggressive periodontitis. Periodontal problems will usually be detected during routine dental checkups.

    Recommendation: document:

    1.  Symptoms. Some patients may have experienced minimal or even no symptoms, however it is likely that they will be aware of bleeding on brushing. Depending on the severity of the disease they may also have noted tooth mobility, gingival recession and sensitivity. In cases of advanced disease, patients may have experienced episodes of infection presenting as pain, swelling and a bad taste in the mouth.

    2.  Family history of periodontal disease. It is acknowledged that eliciting an accurate family history from patients may be challenging for many reasons, from the variable ability for individuals to recall information, to changes in oral health practices and diagnostic criteria over time.

    3.  General health/wellbeing and co-morbidities. Patients with aggressive periodontitis should be systemically healthy. Certain genetic and haematological conditions increase susceptibility to periodontitis, which may follow a more rapid course at a young age, however these are cases fall into a different classification, “Periodontitis as a Manifestation of Systemic < Diseases”< and therefore should not be described as aggressive periodontitis.1 It should however be noted that diabetes mellitus, which is known to increase the risk of periodontitis, is not listed as a systemic disease and therefore these patients may be diagnosed with aggressive periodontitis.

    4.  Age. Although age is not part of the diagnostic criteria, it is recognized that localised aggressive periodontitis disease tends to have circumpubertal onset and generalised aggressive periodontitis mainly occurs in those less than 30 years old.

    5.  Smoking. This has been identified as a significant risk factor for periodontal disease and has been associated with a poor response to treatment.4

    Clinical Examination

    Recommendation: Full mouth periodontal indices (Basic Periodontal Examination, BPE) should be assessed and documented. Recommendation: Where the BPE identifies scores of 3 or 4, a more detailed periodontal examination should be performed.5 This should include six point probing depths around each tooth and recording of the degree of mobility and furcation involvement and recession.

    Clinical examination should involve routine assessment of the oral soft tissues and the use of the Basic Periodontal Examination as screening tool.5 This index identifies patients with periodontal disease as defined by the presence of plaque retentive factors including calculus, increased probing depths, inflammation judged by bleeding on probing, gingival recession and furcation involvement. It does not differentiate between the types of periodontitis.

    It is recommended that in sextants scoring 3 or 4, a more detailed periodontal examination should be performed. Six point probing depths around each tooth, the degree of mobility and furcation involvement should be recorded. This information guides diagnosis by providing information about disease pattern and severity.

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    Severity Assessment

    Recommendation: Assess severity of periodontal disease for each affected tooth using probing or pocket depths according to table 2
    – record the degree of bone loss according to Table 3.
    [Evidence level C]

    According to international guidelines for the classification of periodontal diseases, the severity of disease is characterized on the basis of clinical attachment level (CAL) which is defined relative to the cementoenamel junction (CEJ).1 Clinically this is the distance from the CEJ to the depth of the probable periodontal pocket (Table 1).6

    Table 1 Severity of periodontal disease based on clinical attachment level (CAL)


    CAL (mm)








    It is, however, unusual in clinical practice to measure clinical attachment level. Pocket depths or probing depths are usually recorded, this represents the distance from the gingival margin to the depth of the probable periodontal pocket. Although this measurement is easier to record it is not considered to be valid over time the level of the gingival margin is not a fixed reference point: it may change over time as a result of inflammation or recession. In cases where there has been gingival recession, this measurement (CEJ to gingival margin in mm) can be used together with probing depth to determine CAL. (PD+Recession=CAL)

    Accepting the limitations of the probing depth measurement, a classification of severity based on probing or pocket depths is generally used as follows:

    Table 2 Severity of periodontal disease based on probing or pocket depths


    Probing or Pocket Depth (mm)







    Severity of bone loss should be reported as part of the radiographic findings and graded (Table 3). Other radiographic features of importance include the pattern of bone loss (horizontal or vertical); the teeth affected and furcation involvement.


    Table 3. Criteria for assessing severity of bone loss on radiography.

    Minor bone loss

    ≤ 1 ⁄ 3 of the root length

    Moderate bone loss

    > 1⁄3 and <1⁄2 of the root length

    Severe bone loss

    > 1 ⁄ 2 of the root length

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    Recommendation: No routine blood investigations are required in patients with AgP. If leukaemia is suspected, arrange urgent medical referral. [Evidence level D]

    Recommendation: Radiographic examination should be undertaken on all quadrants that score 3 or 4 in the BPE. [Evidence Level C]

    Guidelines issued by the Faculty of General Dental Practitioners and the European Commission regarding the use of radiographic imaging in periodontal diagnosis are based on expert opinion as a result of insufficient evidence base.7,8 Recommendations of the use of different imaging modalities are based on the degree of periodontal pocketing and distribution throughout the mouth. Radiographs provide information about bone levels and the pattern of bone loss.

    In aggressive periodontitis is usual for bone loss to begin around the first permanent molar teeth and the incisors and the pattern is often symmetrical. This is often visible on periapical radiographs as vertical defects in the molar regions. Anteriorly, however, bone loss may be horizontal due to the thin alveolar contour in this area.9 Additionally, comparison with previous images may be helpful to determine the rate of bone loss. It is acknowledged that this may vary widely between individuals and on a site-by-site basis within the same mouth over time, and there are no guidelines to quantify the rate of bone loss for use as a tool in diagnosis.9

    In clinical practice, the diagnostic criteria relating to immune cell behavior, levels of cytokines and the presence of specific bacteria are of limited use as tests are not commonly available.

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    Non-Antimicrobial Treatment

    Recommendation: patients with aggressive periodontitis should be given written and verbal advice on appropriate methods of toothbrushing and interdental cleaning. [Evidence level A].

    Recommendation: Non-surgical periodontal therapy (NSPT) involving supra and subgingival scaling and root surface debridement using hand scalers and ultrasonic scaling instruments should be provided. [Evidence level D]

    Recommendation: Patients who smoke should be advised to stop smoking. [Evidence level D] Evidence review

    The first treatment modality is cause-related therapy to remove the primary aetiology, bacterial plaque. This involves oral health education,

    including toothbrushing and interdental cleaning instruction to improve plaque control and reduce inflammation. The role of bacterial plaque in gingivitis and periodontitis is long established10 and as a result it is not considered appropriate to conduct clinical trials where the control group has no access to oral hygiene measures. The most recent literature therefore compares the relative effectiveness of different oral hygiene measures in reducing plaque levels, inflammation and probing depths. The majority of these studies involve patients with gingivitis and chronic periodontitis and there are no studies which look at the effect of personal oral care specifically related to the prevention or progress of aggressive periodontitis, however as bacterial plaque is the primary aetiological factor in aggressive periodontitis the findings can be related.

    Much of the information which has driven public oral health messages about brushing twice a day and using interdental cleaning aids is based on longitudinal studies, which show that over a 25 year or more period, bushing more than once a day and keeping plaque scores beneath 20% reduces the risk of tooth loss.11,12 Systematic reviews of randomised controlled trials or controlled trials, show that when professional instruction is given or professional prophylaxis provided in addition to the patient’s usual oral hygiene regimen, this results in small decreases in gingival inflammation.13 Similarly, a systematic review exploring the efficacy of interdental cleaning with floss or interdental brushes over toothbrushing alone, reported minimal benefits in reducing inflammation and probing depths.14 More recently a Cochrane systematic review has identified that oscillating powered toothbrushes are more effective at removing plaque than side-to-side brushes in the short term.15  One of the recurring discussion points of these reviews is that the number of good quality studies is small, especially considering the overall size of the body of literature in this area.

    Non-surgical periodontal therapy (NSPT) for periodontal disease this involves supra and subgingival scaling and root surface debridement using hand scalers and ultrasonic scaling instruments. The aim of this is to further reduce bacterial load and disrupt the subgingival biofilm. Improvement in periodontal condition is measured in the scientific literature using validated indices, which assess the amount of bleeding on probing, plaque on tooth surfaces, probing depths and CAL. The primary outcome measures are generally CAL and probing depth and it is considered that a 2mm improvement16 in these indices is clinically relevant. It should be noted therefore that in most of the studies considered in this review, power calculations were performed based on detection of 1mm change in these indices. As a result the majority of the studies are underpowered to detect a clinically significant difference.

    There is one longitudinal follow up study designed to assess the outcome of NSPT alone in patients with aggressive periodontitis.16  This involved a relatively large number of patients (n=79) and treatment detailed as 4 appointments at which oral hygiene instruction and supra and subgingival debridement and root surface instrumentation were provided, there was no control group. Periodontal indices were reviewed 10 weeks post operatively and improvements in bleeding and plaque scores and mean decreases in probing depths and gains in clinical attachment were described but improvements in mean probing depths were modest (2.11+/-2.01 mm).

    The majority of evidence for the efficacy of NSPT in aggressive periodontitis comes from randomised controlled trials (RCTs) where it acts as the control for NSPT provided with adjunctive antibiotics. These studies mostly show that with NSPT alone periodontal parameters will improve in the 6 months following treatment.17-24 However, studies with a follow up of 6 months or more seem to show that pocket depths and clinical attachment levels are less well sustained than where antimicrobials are provided.17,25 Due to the limited number of studies and the quality of the published information is it not possible to draw conclusions in this regard.

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    Empirical Antimicrobial Treatment

    Empirical antimicrobial therapy is a term used to describe therapy started prior to availability of microbiology results or if a microbiological diagnosis is not going to be possible. Most antimicrobial prescribing for aggressive periodontitis is therefore empirical as microbiological sampling is not part of routine practice.

    Recommendation: systemic antibiotics should be reserved for patients who do not show improvement at review carried out 2-3 months following completion of debridement, where other factors (e.g plaque control) are favourable. They should always be prescribed as an adjunct to NSPT. [Evidence level D]

    Recommendation: first line antimicrobial regimen would be oral Amoxicillin electronic Medicines Compendium information on Amoxicillin 500mg 8-hourly plus oral Metronidazole electronic Medicines Compendium information on Metronidazole 500mg 8-hourly for seven days OR Azithromycin electronic Medicines Compendium information on Azithromycin 500mg OD for 3 days in penicillin allergic patients.
    [Evidence level D]

    Evidence for the efficacy of antimicrobial therapy.
    In an era of increasing antimicrobial resistance it is important to evaluate the efficacy of antimicrobial treatments, and to objectively assess choice of agent, dose and duration in an attempt to minimize harmful effects. The recommendation here reflects the lack of robust evidence for a benefit of adjunctive antimicrobial therapy, while accepting that it has become custom to add antibiotics in this clinical condition.

    Unlike chronic periodontitis, aggressive periodontitis has been associated with the specific bacteria, namely Aggregatibacter actinomycetemcomitans and Porphymonas gingivalis. Both of these bacterial species produce a number of virulence factors and have the ability to invade host tissues, which protects from mechanical NSPT. As a result of this the use of systemic antimicrobials may have role to play, however, convincing evidence of effectiveness from appropriately powered studies is lacking. While some consider that antibiotics should be used as an adjunct to NSPT which reduces overall bacterial load and disrupt the biofilm theoretically making bacteria more susceptible to antibiotics,26 other studies indicate that antibiotics do not reduce the total counts of streptococci.27 Although recent work is lacking, A. actinomycetemcomitans is usually sensitive to Amoxicillin electronic Medicines Compendium information on Amoxicillin, but frequently resistant to macrolides.28

    Table 4 displays keys features of the randomised placebo controlled trials on this subject. These mainly involve patients with generalised aggressive periodontitis, however four trials involving localised aggressive periodontitis were completed in the 1990s. As stated previously the majority of these RCTs are underpowered to detect a difference that would be considered clinically significant. They also use a variety of different antibiotic regimens and have reported the data in different ways. As a result there is no recognised consensus regarding the choice of antibiotic, dosage or timing.

    A systematic review in 2012 combined the data from trials that used a combination of Amoxicillin electronic Medicines Compendium information on Amoxicillin and Metronidazole electronic Medicines Compendium information on Metronidazole as an adjunct to NSPT in a meta-analysis.29 The results suggest that these antibiotics do provide an additional clinical benefit in terms of reducing probing depth and CAL. However, even though there was no heterogeneity detected between the studies, this should be considered with some caution due to the small size of the studies. With such limited follow up it is impossible to know whether the differences achieved with antibiotics are sustained in the longer term.19

    It has been suggested that poor compliance with antibiotic regimens adversely affects the outcome of periodontal treatment.24  Azithromycin electronic Medicines Compendium information on Azithromycin may therefore offer advantages over the more frequently investigated combination of  Amoxicillin electronic Medicines Compendium information on Amoxicillin and Metronidazole electronic Medicines Compendium information on Metronidazole which is  generally prescribed over 7-10 days TDS. When Azithromycin electronic Medicines Compendium information on Azithromycin is prescribed as a 3 day ODS course, serum and gingival concentrations of Azithromycin electronic Medicines Compendium information on Azithromycin remain above the minimal inhibitory concentration for 7 days following administration.30 Unfortunately the amount of evidence for Azithromycin electronic Medicines Compendium information on Azithromycin in treatment of AgP is limited to just one RCT.17

    The harms of antimicrobials, aside from antimicrobial resistance, should also be considered, for example in one trial 30% of patients in the antibiotic test group suffered nausea, diarrhoea or vomiting24 – a significant concern given the modest dental benefits.

    Table 4. Review of studies evaluating the effectiveness of antimicrobial therapy in aggressive periodontitis.




    n test

    n control


    Primary Outcomes


    FU (max)

    Clinical Outcome


    Generalised AgP

    Randomised (2nd phase ofGuerrero2005)
    - not placebo controlled

    Amox 500mg tds
    7/7 and metro
    500mg tds 7/7 vs



    Original groups
    stratified for smoking then
    for in stats model

    Powered to detect 1mmdifference in deep pockets(7mm).

    Not clinically significant
    endpoint. 2 phases
    not blinded in
    second phase, no control group to second phase. so improvements might have occurred without antibiotics.


    Antibiotic group showed improvement in PD (1.4mm in pockets depth
    >7mm) and CAL gain (1mm). Initial treatment group: statistically significant improvement in deep pockets but the changes in other parameters were insignificant.


    Generalised AgP


    Amox 375mg
    +250mg Metro




    Powered to detect a 1mm difference in CAL

    Not clinically significant endpoint.


    Both groups improved with treatment but deep pockets significantly better at 3/12. Improvements in CAL continued in test group at 6/12

    Casarin 201218

    Generalised AgP

    Randomised blinded

    Metro 250mg tds
    +Amox 500mg tds



    Even numbers in each group, not further accounted for

    Powered ton detect a 1mm difference in CAL at deep sites (7mm+)



    Moderate pockets reduced significantly at 6/12 but no difference in deep pockets or CAL

    Varela 201119

    Generalised AgP

    Not Randomized, not blinded

    Amox 250 +
    Metro 250 10 days/

    Dox 200mg then100mg for 14 days



    Even in each group, not further accounted for

    None stated?

    Short follow up 2/12, No power calculation, likely underpowered. High risk of bias.


    Significant improvements in CAL and PPD in AB groups, Amox and Metro sig different to Dox but ≤ 1mm

    Baltaciogl u 201120

    Generalised AgP

    Double- blind, Randomised

    Metro 400mg tds
    + Amox 500mg tds 14/7




    Power calculation based on % difference in bacteria not clinical parameters

    Not powered for clinically relevant outcome


    Significant improvements in PD and CAL (except CAL in shallow sites).

    More pockets reduced to less than 5mm in test group

    Mestnik 201021

    Generalised AgP


    Randomized, not blinded

    500mg 7/7





    >10/day excluded, 3 and 4 in groups. Not further accounted for

    reduction between baseline and 3 months: not quite clear





    Gingival index
    and plaque index – not different between test and control. Gains in CAL and change in PPD sig different c.f. control


    Generalised and Localised AgP

    Randomised, placebo controlled, double blinded

    Azithromycin electronic Medicines Compendium information on Azithromycin 500mg ODS 3/7 vs placebo



    Stratified for smokers

    Powered to detect a 1mm difference in CAL

    Underpowered, Not powered for clinically relevant outcome


    CAL and probing depths Significant improvement in probing depths vs control (mean1mm)

    Haas 200817

    Generalised AgP

    Randomized unblinded

    Met 500mg tds
    7/7 alone, Met+Amo 500mg tds 7/7, Dox 200mg initial then 100mg OD 14/7

    10, 10, 12


    Not stratified for smoking, acknowledged as limitation 3-5 in each group

    No power calculation

    Antibiotics 6 weeks post therapy Underpowered

    4/12 post Abs (6/12 from baseline)

    Bleeding/probing, no difference from control. Metro and M+A groups had sig reduction in pockets >6mm

    Xajigeorgi ou 200623

    Generalised AgP

    Double-blind, Randomis ed

    500mg Amox +500mg Metro TDS 7/7



    Randomisation stratified for smoking

    Powered to detect 1mm difference in deep pockets (7mm)



    Significant improvement in pocket depths and CAL at sites initially measuring

    >7mm, more pockets in test groups reduced to ≤5mm

    Guerrero 200524

    Generalised AgP

    Randomised, blinded

    Dox 200mg 8/7/
    Metro 1g 8/7 / Clindamycin
    600mg 8/7

    12, 15, 11




    Unclear re power calculation and what was primary outcome


    Improved CAL at 24 and 6/12 and decrease in probing depths in metro and clindamycin groups cf control and dox

    Sigusch 2001

    Localised AgP

    Randomised blinded

    1500mg Amox + 750mg Metro 8/7



    Not mentioned

    No power calculation detailed

    Did not consider changes ≤ 2mm as clinically relevant


    Significantly more sites with reduced pocketing and more sites gaining CAL in treatment group

    Tinoco 1998

    Generalised AgP (4) and Localised AgP (15)

    Randomised blinded

    250 mg QDS Tetracyline 14 day

    4, 15


    Not recorded

    No power calculation



    Improvements in probing depths, CAL and BOP better in AB group

    Palmer 1996

    Localised AgP

    Randomised blinded

    Met 200mg TDS 10days/ Teracycline 250mgQDS 12days



    Not recorded

    No power calculation



    No further bone loss. Improvement in periodontal indices but not comparison between groups

    Saxen 1993

    Localised AgP

    Randomised blinded

    100mg Dox 10 days

    8 (4 sites only)

    8 (4 sites only)

    Not recorded

    No power calculation



    No difference

    Asikainen 1990

    Timing of antibiotics in relation to clinical treatment

    Recommendations: In cases of AgP, antibiotics should be prescribed with the second course of NSPT. Antibiotic prescription should be given when debridement is completed, with this occurring within as short a timescale as possible. [Evidence level D]

    A review by Herrera et al 200832 concluded that there was a lack of direct evidence regarding when the course of antibiotics should start in relation to debridement. However, within the scope of their review concluded indirectly, that antibiotics should start on the day of debridement completion. Additionally they emphasised that debridement should be of adequate quality should be completed within as short a timescale as possible, ideally less than 1 week.

    The conclusion above was based in part on the results of two cohort trials run separately but with identical methodologies apart from timing of the antibiotic intervention.33 When the probing depths and CAL changes in each group were compared at 6 month follow up, changes were more significant in the group who received antibiotics at the beginning of treatment. It was suggested that one of the reasons for this is that gingival inflammation enhances the delivery of antibiotic to the periodontal pocket because of the associated increases in the flow of gingival crevicular fluid.

    In 2011, Griffiths completed the second phase of trial,24,31 which saw the original placebo group given the same regimen of oral antimicrobials

    (Amoxicillin electronic Medicines Compendium information on Amoxicillin 500mg tds plus Metronidazole electronic Medicines Compendium information on Metronidazole 500mg tds 7/7) as the test group during their retreatment at 6 months. Both groups showed improvements in PD and CAL gain. The initial treatment group had a statistically significant better improvement in deep pockets (pockets initially  >7mm,  0.9mm  change  P=0.003) than  the  delayed  treatment group,  but  the  differences in  changes  in  other  parameters were insignificant.

    Beliveau et al reported on an ongoing trial involving two cohorts of patients with localised AgP who received NSPT, with antibiotics (Amoxicillin electronic Medicines Compendium information on Amoxicillin 500mg and Metronidazole electronic Medicines Compendium information on Metronidazole 250mg) being prescribed immediately or 3 months following debridement.34 Results of this retrospective study suggest that by prescribing antibiotics immediately, periodontal parameters improve more quickly, however by 6 months both regimens were effective.

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    Directed Antimicrobial Treatment (when microbiology results are known)

    Microbiology sampling is not clinically available for AgP and therefore this is not relevant.

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    Duration of Treatment

    Recommendation: If Amoxicillin electronic Medicines Compendium information on Amoxicillin and Metronidazole electronic Medicines Compendium information on Metronidazole are given 7 days therapy is appropriate, 3 days is appropriate if Azithromycin electronic Medicines Compendium information on Azithromycin is used. [Evidence level D]

    Justification/evidence base

    Table 4 indicates that most studies have used 7-14 days treatment but the choice of duration has been arbitrary. That dosing regimen should be as short as possible, whilst still providing effective therapy. The search of the literature, detailed above (Table 4) reveals no consensus with regards to the duration of antibiotic therapy. There are no studies comparing different durations of the same antibiotic prescription. There is also no consensus as to how long the level of antibiotic needs to remain above the minimum inhibitory concentration following NSPT to be effective.

    If Azithromycin electronic Medicines Compendium information on Azithromycin is prescribed, it has been suggested that a 3 day course of 500mg ODS is effective to produce levels of the drug above the minimum inhibitory concentration for 7-10 days.17,30 For Amoxicillin electronic Medicines Compendium information on Amoxicillin and Metronidazole electronic Medicines Compendium information on Metronidazole, the available RCTs (Table 4) describe several regimens and the choice of these is not evidence based.18-24,31 They also do not provide information about drug concentrations within the periodontal tissues. A recent controlled trial investigated the concentration of antibiotics in the periodontal tissues of patients undergoing periodontal surgery and crown lengthening who were prescribed 500mg amoxicillin and 250mg Metronidazole electronic Medicines Compendium information on Metronidazole for 7 days. The concentrations of both drugs in the gingival tissues were measured at the end of this course of treatment and were reported to be well above the minimum inhibitory concentration required.35 There was no follow up beyond 7 days so it is unclear how long these levels are maintained. This one study does suggest, however, that regimens extending beyond 7 days are not indicated.

    There are increasing concerns about antimicrobial resistance (AMR) and a drive against prescribing antimicrobials where there is a lack of clear evidence of benefit. AMR is a harm that needs to be considered at the time of prescribing and guideline preparation. A seven day course of co- amoxiclav doubled the counts of oral streptococci that were resistant to penicillin, an effect which persisted for many months.27 A single dose of Amoxicillin electronic Medicines Compendium information on Amoxicillin 3g reduces the numbers of penicillin-streptococci in saliva but can also select for penicillin-resistant streptococci.36 RCT evidence indicates that seven days of clarithromycin or three days of Azithromycin electronic Medicines Compendium information on Azithromycin cause a 50% increase in macrolide resistance.37

    Since acute aggressive periodontitis is caused by an imbalance in the normal gingival microbial flora, we advise that courses of antimicrobial therapy should be limited to 7 days for Amoxicillin electronic Medicines Compendium information on Amoxicillin and Metronidazole electronic Medicines Compendium information on Metronidazole and 3 days for Azithromycin electronic Medicines Compendium information on Azithromycin.

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    Switch to oral agent(s)

    Therapy for AgP is generally given orally in the first instance so this is not relevant.

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    Treatment Algorithm

    Clinical algorithms: a summary of treatment protocols is provided in the attached flowchart document “Aggressive Periodontitis Treatment Guideline”

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    Treatment Failure

    Treatment of aggressive periodontitis aims to achieve periodontal stability by reducing overall inflammation, pocket depth and improving clinical attachment levels. Due to the nature of periodontal disease it is not unusual to see that, although overall periodontal health improves following treatment, disease activity continues to persist at isolated sites.

    Clinical indicators of successful treatment could be considered to be based on factors identified as positive predictors for site progression:38-40

    1.  Probing depths ≤5mm
    2.  Bleeding on probing ≤20%
    3.  Absence of suppuration

    An important feature of successful treatment is control of risk factors where possible and these should be followed up, objectively where possible.

    • Full mouth plaque score should be performed and should be maintained at ≥70% Plaque free.
    • Patients should be encouraged to liaise with their medical practitioner to facilitate monitoring of their HbA1C and other relevant indices
    • Smoking cessation advice should be given4 and the patient encouraged to attend their GMP for further advice

    Repeated courses of antibiotics are not indicated to manage aggressive periodontitis where no efforts have been made to control risk factors. Further treatment, involving surgery or local antimicrobials used alongside further subgingival debridement may be indicated if deep pockets (>5mm) and bleeding on probing persist after NSPT as evidence from longitudinal studies suggests that these are more at risk of experiencing further periodontal breakdown in both chronic periodontitis40 and aggressive periodontitis39.

    • Surgery

    Evidence relating specifically to surgery in aggressive periodontitis cases is limited to case reports and case series.41 Results of a meta-analysis in 2005 looking at outcomes in chronic periodontitis, suggest that surgery is indicated where pockets of greater than 6mm in depth persist, as these sites respond to surgical treatment better than to further NSPT.42 Depending on local factors, this could be open flap debridement or regeneration using biomaterials.

    No antibiotics are indicated as prophylaxis for this type of surgery.43

    • Local Antimicrobials

    There have only been two studies comparing the use of local antimicrobials, prescribed as an adjunct to NSPT, with NSPT alone. Both of these describe the first course of treatment rather than treatment targeting sites which have not responded to the initial stage.

    Local antibiotics have advantages in that, as they are deposited directly into the affected periodontal pocket, the risks of adverse effects and antimicrobial resistance are reduced. This method of delivery is particularly appropriate where there are a limited number of sites to be treated, this may be in localized disease or to target residual sites.

    Unsal et al performed a randomized controlled trial involving patients with localized aggressive periodontitis.44 The 2 test groups received subgingival delivery of 1% chlorhexidine gel and 40% tetracycline gel, however, these interventions did not provide any benefit over NSPT alone 3 months after final debridement. The second trial investigated the effect of subgingival tetracycline fibres in comparison to NSPT using a split mouth design in patients with generalized aggressive periodontitis.45 Six months after treatment they reported a statistically significant improvement in probing depths and CAL but these differences amounted to less than 1mm. Given the restricted quality of the literature, it has been suggested that the decision to use local antimicrobials be made on an individual basis rather than it being evidence based.41

    The conclusion of this review is that there is insufficient evidence to support the use of locally delivered antimicrobials in the treatment of aggressive periodontitis in the initial stage of therapy. They may be considered for localised areas of increased probing depths which persist following standard management detailed in this guideline.

    • Maintenance Therapy

    There are no studies regarding the optimal recall intervals for follow up of patients with AgP however it is generally considered that maintenance therapy is key to controlling disease progression and reducing tooth loss.46-48

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    Record: 4917


    • To improve the diagnosis and management of aggressive periodontitis


    • To provide evidence-based recommendations for appropriate diagnosis and investigation of aggressive periodontitis.
    • To provide evidence-based recommendations for appropriate non-antimicrobial management of aggressive periodontitis.
    • To provide evidence-based recommendations for appropriate empirical antimicrobial therapy of aggressive periodontitis.
    • To recommend appropriate dose, route of administration and duration of antimicrobial agents.
    • To advise in the event of antimicrobial allergy.
    • To set-out criteria for referral to specialists.
    Clinical condition:

    Aggressive periodontitis

    Target patient group:
    Target professional group(s): Secondary Care Doctors
    Adapted from:

    Evidence base

    Evidence levels:

    A. Meta-analyses, randomised controlled trials/systematic reviews of RCTs
    B. Robust experimental or observational studies
    C. Expert consensus.
    D. Leeds consensus. (where no national guidance exists or there is wide disagreement with a level C recommendation or where national guidance documents contradict each other)

    1. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999; 4(1): 1-6.
    2. Susin C, Haas AN, Albandar JM. Epidemiology and demographics of aggressive periodontitis. Periodontol 2000 2014; 65(1): 27-45.
    3. Armitage GC. Periodontal diagnoses and classification of periodontal diseases. Periodontol 2000 2004; 34: 9-21.
    4. Hughes FJ, Syed M, Koshy B, et al. Prognostic factors in the treatment of generalized aggressive periodontitis: II. Effects of smoking on initial outcome. J Clin Periodontol 2006; 33(9): 671-6.
    5. Periodontology. TBSo. Basic periodontal examination (BPE). 2011.
    6. Armitage GC. Clinical evaluation of periodontal diseases. Periodontol 2000 1995; 7: 39-53.
    7. Practitioners. FoGD. Selection Criteria for Dental Radiography. 3rd ed; 2013.
    8. European guidelines on radiation protection in dental radiology
      The safe use of radiographs in dental practice 2004
    9. Albandar JM. Aggressive periodontitis: case definition and diagnostic criteria. Periodontology 2000 2014; 65(1): 13-26.
    10. Loe H, Theilade E, Jensen SB. Experimental Gingivitis in Man. Journal of periodontology 1965; 36: 177-87.
    11. Axelsson P, Nystrom B, Lindhe J. The long-term effect of a plaque control program on tooth mortality, caries and periodontal disease in adults. Results after 30 years of maintenance. Journal of clinical periodontology 2004; 31(9): 749-57.
    12. Kressin NR, Boehmer U, Nunn ME, Spiro A, 3rd. Increased preventive practices lead to greater tooth retention. Journal of dental research 2003; 82(3): 223-7.
    13. van der Weijden GA, Hioe KP. A systematic review of the effectiveness of self-performed mechanical plaque removal in adults with gingivitis using a manual toothbrush. Journal of clinical periodontology 2005; 32 Suppl 6: 214-28.
    14. Slot DE, Dorfer CE, Van der Weijden GA. The efficacy of interdental brushes on plaque and parameters of periodontal inflammation: a systematic review. International journal of dental hygiene 2008; 6(4): 253-64.
    15. Deacon SA, Glenny AM, Deery C, et al. Different powered toothbrushes for plaque control and gingival health. The Cochrane database of systematic reviews 2010; (12): CD004971.
    16. Hughes FJ, Syed M, Koshy B, et al. Prognostic factors in the treatment of generalized aggressive periodontitis: I. Clinical features and initial outcome. J Clin Periodontol 2006; 33(9): 663-70.
    17. Haas AN, de Castro GD, Moreno T, et al. Azithromycin as an adjunctive treatment of aggressive periodontitis: 12-months randomized clinical trial. J Clin Periodontol 2008; 35(8): 696-704.
    18. Casarin RC, Peloso Ribeiro ED, Sallum EA, Nociti FH, Jr., Goncalves RB, Casati MZ. The combination of amoxicillin and metronidazole improves clinical and microbiologic results of one-stage, full-mouth, ultrasonic debridement in aggressive periodontitis treatment. J Periodontol 2012; 83(8): 988-98.
    19. Varela VM, Heller D, Silva-Senem MX, Torres MC, Colombo AP, Feres-Filho EJ. Systemic antimicrobials adjunctive to a repeated mechanical and antiseptic therapy for aggressive periodontitis: a 6-month randomized controlled trial. J Periodontol 2011; 82(8): 1121-30.
    20. Baltacioglu E, Aslan M, Sarac O, Saybak A, Yuva P. Analysis of clinical results of systemic antimicrobials combined with nonsurgical periodontal treatment for generalized aggressive periodontitis: a pilot study. Journal 2011; 77: b97.
    21. Mestnik MJ, Feres M, Figueiredo LC, Duarte PM, Lira EA, Faveri M. Short-term benefits of the adjunctive use of metronidazole plus amoxicillin in the microbial profile and in the clinical parameters of subjects with generalized aggressive periodontitis. Journal of clinical periodontology 2010; 37(4): 353-65.
    22. Yek EC, Cintan S, Topcuoglu N, Kulekci G, Issever H, Kantarci A. Efficacy of amoxicillin and metronidazole combination for the management of generalized aggressive periodontitis. J Periodontol 2010; 81(7): 964-74.
    23. Xajigeorgiou C, Sakellari D, Slini T, Baka A, Konstantinidis A. Clinical and microbiological effects of different antimicrobials on generalized aggressive periodontitis. J Clin Periodontol 2006; 33(4): 254-64.
    24. Guerrero A, Griffiths GS, Nibali L, et al. Adjunctive benefits of systemic amoxicillin and metronidazole in non-surgical treatment of generalized aggressive periodontitis: a randomized placebo-controlled clinical trial. J Clin Periodontol 2005; 32(10): 1096-107.
    25. Sigusch B, Beier M, Klinger G, Pfister W, Glockmann E. A 2-step non-surgical procedure and systemic antibiotics in the treatment of rapidly progressive periodontitis. Journal of periodontology 2001; 72(3): 275-83.
    26. Mombelli A. Heresy? Treatment of chronic periodontitis with systemic antibiotics only. J Clin Periodontol 2006; 33(9): 661-2.
    27. Cremieux AC, Muller-Serieys C, Panhard X, et al. Emergence of resistance in normal human aerobic commensal flora during telithromycin and amoxicillin-clavulanic acid treatments. Antimicrobial agents and chemotherapy 2003; 47(6): 2030-5.
    28. Madinier IM, Fosse TB, Hitzig C, Charbit Y, Hannoun LR. Resistance profile survey of 50 periodontal strains of Actinobacillus actinomyectomcomitans. J Periodontol 1999; 70(8): 888-92.
    29. Sgolastra F, Petrucci A, Gatto R, Monaco A. Effectiveness of systemic amoxicillin/metronidazole as an adjunctive therapy to full-mouth scaling and root planing in the treatment of aggressive periodontitis: a systematic review and meta-analysis. Journal of periodontology 2012; 83(6): 731-43.
    30. Blandizzi C, Malizia T, Lupetti A, et al. Periodontal tissue disposition of azithromycin in patients affected by chronic inflammatory periodontal diseases. J Periodontol 1999; 70(9): 960-6.
    31. Griffiths GS, Ayob R, Guerrero A, et al. Amoxicillin and metronidazole as an adjunctive treatment in generalized aggressive periodontitis at initial therapy or re-treatment: a randomized controlled clinical trial. J Clin Periodontol 2011; 38(1): 43-9.
    32. Herrera D, Alonso B, Leon R, Roldan S, Sanz M. Antimicrobial therapy in periodontitis: the use of systemic antimicrobials against the subgingival biofilm. Journal of clinical periodontology 2008; 35(8 Suppl): 45-66.
    33. Kaner D, Christan C, Dietrich T, Bernimoulin JP, Kleber BM, Friedmann A. Timing affects the clinical outcome of adjunctive systemic antibiotic therapy for generalized aggressive periodontitis. J Periodontol 2007; 78(7): 1201-8.
    34. Beliveau D, Magnusson I, Bidwell JA, et al. Benefits of early systemic antibiotics in localized aggressive periodontitis: a retrospective study. Journal of clinical periodontology 2012; 39(11): 1075-81.
    35. Amid R, Tabeie MB, Kadkhodazadeh M, Mehdizadeh AR, Youssefi N. Local concentration of systemic amoxicillin and metronidazole in healthy and inflamed gingiva: a comparative in vivo study. Drug metabolism and drug interactions 2012; 27(2): 113-8.
    36. Southall PJ, Mahy NJ, Davies RM, Speller DC. Resistance in oral streptococci after repeated two-dose amoxycillin prophylaxis. J Antimicrob Chemother 1983; 12(2): 141-6.
    37. Malhotra-Kumar S, Lammens C, Coenen S, Van Herck K, Goossens H. Effect of azithromycin and clarithromycin therapy on pharyngeal carriage of macrolide-resistant streptococci in healthy volunteers: a randomised, double-blind, placebo-controlled study. Lancet 2007; 369(9560): 482-90.
    38. Armitage GC. Periodontal diseases: diagnosis. Annals of periodontology / the American Academy of Periodontology 1996; 1(1): 37-215.
    39. Matuliene G, Pjetursson BE, Salvi GE, et al. Influence of residual pockets on progression of periodontitis and tooth loss: results after 11 years of maintenance. Journal of clinical periodontology 2008; 35(8): 685-95.
    40. Claffey N, Egelberg J. Clinical indicators of probing attachment loss following initial periodontal treatment in advanced periodontitis patients. Journal of clinical periodontology 1995; 22(9): 690-6.
    41. Teughels W, Dhondt R, Dekeyser C, Quirynen M. Treatment of aggressive periodontitis. Periodontology 2000 2014; 65(1): 107-33.
    42. Heitz-Mayfield LJ. How effective is surgical therapy compared with nonsurgical debridement? Periodontology 2000 2005; 37: 72-87.
    43. Guidelines for the Antibiotic Prophylaxis for Periodontal Surgery: Leeds Health Pathways 2013
    44. Unsal E, Walsh TF, Akkaya M. The effect of a single application of subgingival antimicrobial or mechanical therapy on the clinical parameters of juvenile periodontitis. Journal of periodontology 1995; 66(1): 47-51.
    45. Sakellari D, Vouros I, Konstantinidis A. The use of tetracycline fibres in the treatment of generalised aggressive periodontitis: clinical and microbiological findings. Journal of the International Academy of Periodontology 2003; 5(2): 52-60.
    46. Baumer A, Pretzl B, Cosgarea R, et al. Tooth loss in aggressive periodontitis after active periodontal therapy: patient-related and tooth- related prognostic factors. Journal of clinical periodontology 2011; 38(7): 644-51.
    47. Gunsolley JC, Califano JV, Koertge TE, Burmeister JA, Cooper LC, Schenkein HA. Longitudinal assessment of early onset periodontitis. Journal of periodontology 1995; 66(5): 321-8.
    48. Mros ST, Berglundh T. Aggressive periodontitis in children: a 14-19-year follow-up. Journal of clinical periodontology 2010; 37(3): 283-7.

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