CONTENTS

INTRODUCTION
CHARACTERISTIC FEATURES OF AGGRESSIVE PERIODONTITIS.
PRINCIPLES OF THERAPEUTIC INTERVENTION
THERAPEUTIC GOALS
GENERAL PRINCIPLES IN TREATING AGGRESSIVE
PERIODONTITIS
TREATMENT CONSIDERATION
INITIAL TREATMENT
ANTIBIOTIC THERAPY
ANTIBIOTIC THERAPY AND NON-SURGICAL TREATMENT
ANTIBIOTIC THERAPY AND SURGICAL TREATMENT
SURGICAL MANAGEMENT
GRAFTING PROCEDURES
TOOTH TRANSPLANTATION
OTHER DENTAL CONSIDERATIONS
CURRENT APPROACH
PROGNOSIS
CONCLUSION
REFERENCES
INTRODUCTION
Destructive periodontal diseases affecting the connective tissue attachment and alveolar
bone supporting the teeth have long been considered the principle cause for tooth loss.
According to new classification of 1999, all form of periodontitis, resulting in significant
attachment loss, irrespective of the age of individual are termed as aggressive periodontitis. It
generally affects systemically healthy individuals more in 30 year, although patient may be older.
It may be universally distinguished from chronic periodontitis by the age of onset, the
rapid rate of disease progression, the nature and composition of the associated subgingival
microflora, alteration in the host immune response and a familial aggregation of disease
individuals.
The hallmark of aggressive periodontitis is clinical presentation of periodontal disease
early in the life of the individual. This implies that etiologic agents have been able to cause
clinically detectable levels of disease over a relatively short period of time. This fact in central to
the current understanding of the disease, since it implies infection with a highly virulent
microflora or high level of subject susceptibility to periodontal diseases.

PRINCIPLES OF THERAPEUTIC INTERVENTION

Treatment of Aggressive Periodontitis should only be initiated after completion of a
careful diagnosis by a specifically trained periodontist.
Successful treatment of Aggressive Periodontitis is considered to be dependent on (1)
early diagnosis, (2) dissecting therapy towards elimination or Suppression of the infecting
microorganisms and (3) Providing an environment conducive to long term maintenance.

THERAPEUTIC GOALS
1. To alter or eliminate the microbial etiology and contributing risk factors.
2. Arresting / slow down the progression of disease.
3. Preserving the dentition in comfort, functions and appropriate esthetics.
4. To prevent the recurrence of diseases.
5. Regeneration of the periodontal attachment apparatus.

The goal of therapy to halt the bacterial process and to achieve a more favorable balance
between the bacteria and the host, so that conventional therapy may be more predictably applied.
TREATMENT CONSIDERATION
These cases are often difficult to control and suffer frequent relapses. Since they represent
a very small percentage of total cases seen in the average general dental office and since they
require advanced diagnostics and therapy, these cases should be referral to specialist.
Several general principles apply to these cases
1. These cases are often associated with alteration in host defense; the therapy should begin
by exploring factors that may contribute to changes in the defense system.
At present we can’t alter the genetic factor, it is valuable to inquire about tooth has
pattern in the patient’s family. A family history of severe / early onset periodontitis will
provide a basis for close monitoring of the patient as well as early intervention in other
family members. Non-genetic factors, including smoking, viral infections and prolonged
stress have been shown to produce substantial alteration in host defense. Since these
factors are modifiable, they should be assessed and managed as part of the therapy.

2. The lack of a strong association between plaque accumulations and disease severity in
the aggressive periodontitis and the host alterations noted above often mean that there
patients are less responsive to conventional periodontal therapy (SRP).
This does not mean that plaque control is unimportant, but rather that more
specific approaches to controlling the bacterial challenge may be necessary. Future
therapies directed at strengthening the host response may provide new opportunities for
managing these diseases.
3. Surgery may no be advisable in aggressive periodontitis until the infection is
undercontrol.
In most cases of severe and rapidly progressing disease, an altered host defense
may make the response to surgery unpredictable. JP appears to be an exception to this
principle. The altered host statuses frequently interfere with the patient’s response to
periodontal surgery and surgery very these face not be indicated in these patients until
active infection process is under control.

TREATMENT CONSIDERATION
In general, treatment methods for the aggressive periodontitis disease may be similar to those
used for chronic periodontitis with advanced loss of periodontal support. These include
1. Instruction, reinforcement of evaluation of the patient’s plaque control should be
performed.
2. Supra and subgingival scaling and root planning should be performed to remove microbial
plaque and calculus.
3. Local factors contributing should be eliminated or controlled.
a. Removal / relapsing of restorative overhangs and over contoured crowns
b. Correction of ill fitting prosthetic appliances
c. Restoration of carious lesion
d. Odontoplasty
e. Tooth movement
f. Restoration of open contacts which have resulted in food impactions
g. Restorative of occlusal trauma
h. Extraction of hopeless teeth.

4. For reasons of health, lack of effectiveness or non compliance with plaque control, patient
desires at therapist’s decision, appropriate restorative to the disease may be deferred or
delivered.
DECISION PATHWAY

Periodontal disease No

Yes
Prophylaxis monitoring
Treatment SRP,
Local / systemic antibiotic treatment
Nonsurgical/surgical treatment
Re-Evaluation

Stable Not stable

Maintenance & monitoring localised generalized

Microbial assessment

Local treatment systemic treatment

Re-evaluation

Stable Not-stable

Maintenance host change miscellanea

& monitoring factors antibiotic treatment

Stable Not stable

 A. LOCALIZED AGGRESSIVE PERIODONTITIS:
Because the primary organisms in these cases is A a comitans. Conventional therapy
directed at removing plaque and calculus has had little success.
General two approaches to successful therapy are possible (depending on the preference of the
practitioner and the patient)
1. Treatment with the aid of microbial information
Pretreatment microbial samples are taken and DNA robe analysis appears optimal.

MICROBIAL CULTURE

A a comitans + no black pigmented bacteria A a comitans + one of Pg / Pi

( P.g or P.i)

SRP + Doxycycline-100 mg BID (21 days) surgical access + Doxycycline as the first
Chlorhexidine rinse 2 times / day phase of therapy

Microbial evaluation 4-6 wks after

antibiotic therapy

Stable Unstable
SPT or regenerative surgical access + 2nd course
therapy considered systemic antibiotics

2. Treatment without the aid of microbial information

The clinician can assume that microorganism present will be sensitive to a member of the
tetracycline family of antibiotics. Surgery is carried out in conjunction with the regimen of
antibiotics and antimicrobial previously described. SPT follows and can be accompanied by
DNA probes or microbiologic monitoring if clinical or radiographic signs of the disease recur.
ANTIMICROBIAL THERAPY
Mainly tetracycline & derivatives used because
1. A a comitans is sensitive to tetracycline.
2. Concentration in GCF is 10 times greater than serum
3. Possess anticollagenase activity
4. Inhibits osteoclastic bone resorption.

Novak et al (1988) evaluated tetracycline alone plus supragingival plaque control in a 4

LJP patients (dosage-250mg/dl, 3-6 wks). At 3 months assessment 69 % showed gain
attachment, 79% showed decreases pocket depth >2mm & radiographic evidence of an
increase in bone levels.
Systemic antibiotics should only be administered as an adjunct to mechanical debridement
because in undisturbed subgingival plaque. The target organisms are effectively protected
from the antibiotic agents due to the biofilm effect.

To incorporate systemic antibiotics in the treatment of Aggressive Periodontitis a staged

approach to the initial therapy is recommended (Lindhe 4th edition)

Mechanical therapy (SRP) + meticulous oral hygiene

Clinically re assessed after 4-6 weeks

Decision made to gains access to deep lesion (surgery)

& appropriate antibiotics selection based on culture sensitivity tests.

Systemic antibiotics should be administered immediately after completion of surgical

intervention or after 2nd around of mechanical therapy to disrupt biofilm as much as possible.
Microbiology testing may be repeated at 1-3 months after completion of therapy to verify the
estimation or marked suppression of putative pathogen. After resolution of the periodontal
infection the patient should be placed as an individually tailored SPT.
Optimal plaque control by the patient is of paramount importance for a favorable clinical
and microbiologic response to therapy.
Recurrence of disease is an indication
o For a repetition of microbiologic tests.
 o For re-evaluation of the host immune response and
o Re assessment of local and systemic modifying factors.

Monotherapy with systemic antibiotics an adjuvant to mechanical periodontal treatment

can suppress the total subgingival bacterial load and may induce a significant change in the
composition of the subgingival microflora. Antibiotic therapy with single antibiotics agent can’t
predictably eliminate periodontal pathogen. So combination therapy is appropriate. Antibiotics
should not the administered systemically before completion of thorough mechanical debridement.
It’s recommended to start drug administration immediately following a mechanical re-
instrumentation.

ANTIMICROBIAL THERAPY + NON SURGICAL THERAPY

A combination of SRP with systemic tetracycline therapy has been shown to be effective
treatment for control of LJP
Slots and Rosling (1983) compared the clinical and microbiological effects of subgingival
debridement, topical betadine and systemic tetracycline during the different stages in the
management of Localised aggressive periodontitis. Both subgingival debridement and
tetracycline therapy significantly reduced A a comitan an capnocytophagia, but more
profound effect was observed after tetracycline. Topical betadine solution had no effect on the
plaque microflora. Tetracycline treatment produced a slight gain in attachments.

Novak et al (1991) used tetracycline 250 mg qid for 42 days in 4 patients and there was
reductionin pocket depth clinical attachment loss & bleeding on probing in tetracycline + SRP
group for upto 4 years.
Saxen and Asikainen (1993) using either metronidazole or tetracycline 250 mg qid for 12 days
in 27 patients obtained best clinical results with Metronidazole 200 mg tid / 10 days adjunct to
SRP. A a comitans eliminated in 100% of Metronidazole group, in 44 % of tetracycline group and
76% of SRP group.
Christerson and Zambon (1993) in 6 patients used tetracycline 250 mg qid until 1 week after
A a comitans undectable or for a maximum of 8 wks adjunct to SRP and followed up for 24
months. There was improvement in clinical parameters. 4/6 patients were A a comitans positive
after 12 months.
The clinical attachment level increased (0.3+/- 0.3 mm) when Metronidazole 250 mg tid 7
days used adjunct to SRP v/s control using SRP alone. (Yilmaz et al 1996).
 Siguschi(2001) in 18 pateints used metronidazole 500mg bid/8 days, doxycycline 100mg
bid loading dose / 8 days and clindamycine 150 mg qid/8 days adjunct to SRP v/s control. After
24 months there was decrease in gingival index, pocket depth and increased attachment level in
Metronidazole>clindamycine>doxycyxcline.

Genco and co worker (1981) treated LJP with SRP+ tetracycline (250 mg, 14 days every 8
weeks). Measurements of vertical defects were made at intervals of upto 18 months. Bone loss
had stopped and 1/3rd of defects demonstrated on increased in bone level where as in control
group bone loss continued.

The advantages of tetracycline in localised aggressive periodontitis are

1. broad spectrum bacteriostatic antibiotic
2. Specific for LAP associated pathogen
3. Increased concentration in GCF
4. Affinity for saliva coated enamel and inflammatory tissue
5. May suppress bone and fibrinolytic activity
6. Anticollagenase activity

Additional benefits of doxycycline include

1. Lower dosage taken (BID).
2. Not inhibited by with calcium.
3. Does not induce photosensitivity.
4. Decreased GI side effects.
5. Excreted in a tissue rather than kidney.

LOCAL DRUG DELIVER

Goodson (1985) used tetracycline fiber (hollow fiber with tetracycline impregnated ethyl
vinyl acetate) to treat 12 site in 4 patients with localized disease. This approach delivers high
concentration without optimum toxicity & has bactericidal effect. The organism remained
detectable in the pocket 28 day later and actually increased significantly in some cases.
It was not known if the sites in question were repopulated from the surrounding tissue due
to the inability of tetracycline to sufficiently penetrate the tissue or if repopulation may have
occurred from other potential reservoirs in the mouth.
ANTIMICROBIAL THERAPY AND SURGICAL MANAGEMENT

The combination of flap surgery and systemic antimicrobial therapy (tetracycline) was
first reported in 1979 (Baer and Socransky 1970)
This combined approach is a very effective means of treating Localised aggressive periodontitis.
Lindhe and Liljenberg (1984) treated 16 Localised aggressive periodontitis patients with
tetracycline, 250 mg, qid for 14 days and modified Widman flap. Initially this combination of
treatment halted the disease progression, but there was recurrence in 4 patients. These 4 were
retreated in the same manner. The patients were monitored for 5 years and at the end of this
period there was an improvement in all clinical measures with radiographic evidence of bone
fill.

Lindhe (1981) used tetracycline 250 mg qid / 14 days plus surgery in 16 patients. At the end
of 24 months 25 % of patients had recurrent disease activity.
Karnman and Robertson(1985) using tetracycline 250 mg qid for 28 days along with surgery
and SRP in 8 patients. Tetracycline + SRP group showed better than SRP alone in sites with A a
comitans.
Mandell and Socransky (1988) used doxycycline 100 mg bid for 14 days along with surgery
in 8 patients. At the and of 12 months doxycycline + surgery suppressed A a comitans & arrested
disease activity in 6/8 patients.
The mean clinical attachment loss also decreased when tetracycline used adjunct with SRP +
surgery v/s SRP + surgery (Haffajee 1995, Palmer 1983).
Tinoco et al (1998) using combination of amoxicillin and Metronidazole along with SRP and
modified Widman flap surgery for 12 months showed increased in clinical attachment level gain
> 2 mm.

SURGICAL MANAGEMENT (FLAP SURGERY ALONE)

Recommended to gain access to the subgingival microflora and to remove granulation
tissue and infected connective tissue.
In a retrospective study (Waerhaug – 1977), patient with Localised aggressive
periodontitis were successfully treated with supra and subgingival plaque control and scaling.
Flap surgery was undertaken as those sites with a PD > 5 mm. These points were kept under
review for a period of 8-34 years, showed marked improvement in various clinical measures
These results were confirmed by Server et al (1986). In this study 20 Localised
aggressive periodontitis patient were reexamined after 6-12 year after initial therapy
 Mendel et al (1986) compared tetracycline delivery via monolithic fibers, surgery plus
doxycycline (14 days) and doxycycline (14 deep) without surgery in the treatment of localised
aggressive periodontitis. Only the surgery plus doxycycline group was effective in suppressing or
eliminating A a comitans.

GRAFTING PROCEDURES
Various have grafts are used to treat the angular bony defects in LJP.
1. Autogenous bone chips (Oshrains and Kaslick – 1981)
2. Osseous coagulum (Burnette and Steroark - 1969)
3. Frozen autogenous hip marrow (De Marco and Scaletter – 1970)
4. FDBA + tetracycline (Yukna and sepe - 1982)

Any bone graft materials can be used.

Good results are obtained when graft in combined with tetracycline.
The drug should be given systemically and can be incorporated in the graft material.
The GTR procedure is useful in the treatment of local defects associated with LJP.

Mabry et al –1985 demonstrated greater defect fill using systemic and locally delivered
tetracycline with FDBA v/s 3 other treatment regiments (systemic tetracycline + debridement, no
antibiotics + FDBA, no antibiotic + debridement).

TOOTH TRANSPLANTATION
1st advocated by Baer and Gamble (1966).
If permanent under is so severely affected that the only treatment is extraction. The unerupted
teeth in replaced in such cases.
The criteria for successful transplantation are as follows,
1. 3rd molar crown should be slightly smaller than the tooth it is replacing.
2. Root development of the 3rd molar should be incomplete.
3. The transplanted tooth should be kept out of occlusion for 3-4 weeks post
transplantation.

In a 7 year follow up study by Borroing-Moller and Frandsen (1978) 15 transplanted cases

showed that all the teeth survived clinically, none of the teeth as pocket depth >3 mm, no
attachment loss and radiographs evidence of repair of the osseous defects.
Limitation: Root resorption and pulpal death

Advantage: Acts as space maintainer until the patient in old enough for a more permanent
prosthesis.

OTHER DENTAL CONSIDERATIONS IN LOCALISED AGGRESSIVE

PERIODONTITIS.

1. The extensive alveolar bone loss that may lead to pulpal death and exposure of the lateral
root canal - RCT is indicated if the tooth to be saved.
2. Root amputation
3. Hemisection

The objective is an attempt to provide esthetics, phonetics, and functions commensurate with
comprehensive dental health.
Require endodontics and prosthodontics evaluation and support.

CURRENT APPROACH
Earlier the disease is diagnosed, the more conservative the therapy and more predictable
the outcome.
In almost all cases, Tetracycline (250 mg QD) at least 1 week) should be given.
If surgery is indicated then antibiotics should be started approximately 1 hr. before surgery.
Doxy-100 mg/day – can be used
Chlorhexidine rinses – to augment plaque control
In refractory Localised aggressive periodontitis cases, tetracycline resistant actinobacillus species
suspected. After performing antibiotic susceptibility test, consider a combination of amoxillin 375
and metronidazole 250 mg tid for 7 day (Van Winkel et al 1989)

GENERALIZED AGGRESSIVE PERIODONTITIS

In these cases A a comitans is usually present, but other suspected pathogens may be
involved. Microbial analysis in recommended before therapy and at each re-evaluation until
clinical and radiographic stability have been achieved.
Goal of treatment: elimination of the suspected pathogen which requires systemic antibiotics
adjunct to mechanical therapy.

A a comitans Metronidozole-250 mg / Amoxillin-375 mg.

Metronidazole / ciprofloxacin,
Tetracycline.

P. gingivalis Azithromycin 500mg OD / 3-5 days.

P. gingivalis, P.intermedia Tetracycline 250mg QID, 14-21 days.

Black pigmented bacteria Metronidozole-250 mg TID/QID, 10 days.

& spirochetes

Gram positive organisms amoxicillin-clavulanate potassium (Augmentin)

250/500 mg + 125 mg; TID, 10 days.
Gram negative organisms clindamycin 150-300 mg, QID/10n days.

Non-oral gram negative facultative rods,

Pseudomonas, staphylococcus. Ciprofloxacin.

PROGNOSIS
Affected by
1. Extent & location of bone loss.
2. Morphology of bone defects.
3. Crown / root ratio.
4. Degree of mobility.
5. Occlusal factors.
6. Oral hygiene efforts.
7. General health & attitude of the patients.
CONCLUSIONS
Although several options are available for the treatment of localized aggressive
periodontitis, the combination of systemic tetracycline (2–4 weeks course) with flap surgery or
root debridement appears to be the most predictable. Perhaps surgery and tetracycline is the best
option as the procedure involves the removal of granulation and connective tissue infected with
Aa comitans. The cases that do not respond to this management may well benefit from the
combination of metronidazole, amoxillin and root surface debridement. It has been advocated
that microbiological testing should be carried when antimicrobials are being considered for the
treatment of aggressive periodontitis.
 REFERENCES

1. Clinical periodontology by Carranza, 9th edition.

2. Clinical periodontology and implant dentistry, Lindhe 4th edition.

3. Fundamentals of periodontics, Wilson and Kornman

4. Drug, Disease and periodontium, Seymour.

5. Parameters on aggressive periodontitis. J.P 2000: 71: 867-869 (suppl)

6. Rationale for use of antibiotics in periodontics.

J.P- 2002; 73: 188-1196

7. IDJ – 2004; 54: 8-14.

8. J.P – 1996; 67: 831-838

9. Annals of periodontology – 2003; 8: 115-181

10. JCP – 2002; 29(suppl-3): 136-159

11. Periodontal literature reviews – 1996.