aggressive periodontitis, aetiopathogenesis, clinical features,

1. AGGRESSIVE
PERIODONTITIS
PRESENTED BY:
PRABLEEN ARORA
MDS STUDENT

2.  Periodontitis is an infection that can have
many different clinical presentations.
 Aggressive Periodontitis (AgP) comprises
of a group of rare, often severe, rapidly
progressive forms of periodontitis often
charaterized by an early age of clinical
manifestation and a distinctive tendency
for cases to aggregate in families.

3. HISTORICAL BACKGROUND
 1923, Gottlieb reported a patient with fatal case of
epidemic influenza and a disease he called “diffuse
atrophy of alveolar bone”.
 Characterized by Loss of collagen fibres in PDL and
their replacement by loose connective tissue & extensive
bone resorption; leading to widened PDL space.
 1928: Gottlieb attributed it to inhibition of continuous
cementum formation (considered essential for
maintenance of PDL fibres).
 He termed it “deep cementopathia”; this was a disease
of eruption.

4.  1938: Wannenmacher described incisor-first molar presentation
and called it “parodontitis marginalis progressive”.
 Many authors (Goldman 1947 , Gottlieb 1923) considered this to
be degenerative, non inflammatory disease process and gave it the
name “periodontosis”.
 1966: World Workshop in Periodontics concuded that the concept
of “periodontosis” as a degenerative entity was unsubstantiated and
the term should be eliminated from periodontal nomenclature.
 “Juvenile Periodontitis”: given by Chaput & colleagues in 1967
and Butler in 1969.
 1971: Baer defined it as a ‘disease of the periodontium occuring in
an otherwise healthy adolescent which is characterized by a rapid
loss of alveolar bone about more than one tooth of permanent
dentition.

5.  1989: World Workshop in Clinical Periodontics categorized
the disease as Localised Juvenile Periodontitis(LJP), a subset
of broad classification of early-onset periodontitis (EOP).
 Under this classification system, age of onset and distribution
of lesions were of primary importance when making a
diagnosis of LJP.
 More recently, disease with the characteristics of LJP has been
renamed as LOCALIZED AGGRESSIVE PERIODONTITIS
(LAP).
 In the 1999 Classification Workshop of the American
Academy of Periodontology , a consensus report adopted the
term aggressive periodontitis as a new name for this unique
disease classification, replacing the term early-onset
periodontitis.

6. CLASSIFICATION AND CLINICAL
SYNDROMES
Aggressive forms of periodontal disease have been
defined based on the following primary features.
Lang et al (1999):
 Non contributory medical history
 Rapid attachment loss and bone destruction.
 Familial aggregation of cases.

7. SECONDARY FEATURES
 Amounts of microbial deposits inconsistent with the severity of
periodontal tissue destruction.
 Elevated proportions of Aggregatibacter actinomycetamcomitans
and in some Far East populations, Porphyromonas gingivalis.
 Phagocyte abnormalities.
 Hyper-responsive macrophage phenotype, including elevated
proportions of PGE2, IL-1b.
 Progression of attachment loss and bone loss may be self arresting.

8. Subclassification of AgP
(International classification
Workshop)
By Lang et al (1999) ; Tonetti & Mombelli (1999)
Localised aggressive periodontitis (LAP)
 Circumpubertal onset
 Localised first molar/incisor presentation with interproximal
attachment loss on atleast two permanent teeth, one of which
is a first molar, and involving no more than two teeth other
than first molars and incisors.
 Robust serum antibody response to infecting agents.

9. CLINICAL & RADIOGRAPHIC PICTURE OF
LAP

10.  A striking feature is lack of clinical inflammation
despite the presence of deep periodontal pockets and
advanced bone loss.
 Plaque on the affected teeth is minimal.
 The plaque that is present forms a thin biofilm on the
teeth and rarely mineralizes to form calculus.

11. Other clinical features:
1. Distolabial migration of maxillary incisors with
diastema formation.
2. Increasing mobility of maxillary and mandibular
incisors and first molars.
3. Sensitivity to denuded root surfaces to thermal
and tactile stimuli.
4. Deep dull radiating pain during mastication
probably caused by irritation of the supporting
structures by mobile teeth and impacted food.

12. Radiographically
 Vertical loss of alveolar bone around the first molars and
incisors beginning around puberty- classic diagnostic sign of
LAP
 Arc shaped loss of alveolar bone extending from distal surface
of second premolar to mesial surface of second molar.

13. The following possible reasons for the limitation of periodontal
destructon to certain teeth have been suggested:
1. After initial colonization of first permanent teeth to erupt,
A.a evades the host defences by different mechanisms
including production of PMN chemotaxis-inhibiting factors,
endotoxins, collagenases, leukotoxins and other factors that
allow the bacteria to colonize the pocket and initiate
destruction of periodontal tissues.
 After this initial attack, adequate immune defenses are
stimulated to produce opsonic antibodies.
to enhance the clearence and phagocytosis of invading
bacteria and neutralise leukotoxic activity.
 In this manner, colonization of other sites may be
prevented.

14. 2. Bacteria antagonistic to
Aggregatibacter actinomycetamcomitans
colonize the periodontal tissues and inhibit
Aggregatibacter actinomycetamcomitans from further
colonization therefore localizing A.a infection and tissue
destruction.
3. Aggregatibacter actinomycetamcomitans may lose its
leukotoxin-producing ability; progression becomes arrested
or impaired and colonization of new sites may be averted.
4. A defect in cementum formation may be responsible for
localization of lesions.

15. GENERALIZED AGGRESSIVE
PERIODONTITIS (GAP)
 Usually affecting persons< 30 yrs; may be older.
 Generalized interproximal attachment loss affecting atleast
three permanent teeth other than first molars and incisors.
 Pronounced episodic nature of destruction of attachment and
alveolar bone.
 Poor serum antibody response to infecting agent.

16. Two types of gingival responses seen:
1.Severe,acutely inflamed tissues, often proliferating, ulcerated
and fiery red.
(DESTRUCTIVE STAGE )
Bleeding may be spontaneous or with slight stimulation.
Suppuration may be an important feature.
2. Tissues may appear pink, free of inflammation, and
occasionally with some degree of stippling.
Page and Schroeder believed that this type of response
coincides with periods of quiescence in which bone levels
remain stationary.
Systemic manifestations can be seen like fever, weight loss,
mental depression, and general malaise.

17. Radiographically
 Can range from severe bone loss associated with
minimum number of teeth to advanced bone loss
affecting the majority of teeth in the dentition.

18. EPIDEMIOLOGY
 All available investigations, however, indicate that early
onset (aggressive) forms of periodontal diseases are
detectable in all age and ethnic groups (Papapanou
1996).
 51.5% affected individuals.
 These differences are probably due to differences in the
employed epidemiological methodologies and definition
of EOP.

19. PRIMARY DENTITION
 Little evidence is available concerning the prevalence of
Aggressive periodontitis affecting the primary dentition.
 In the few studies from industrialized countries, marginal
alveolar bone loss has been found to affect the primary
dentition of 5 to 11 year olds with frequencies ranging from
0.9-4.5% of subjects (Sweeney et al. 1987).
 More severe cases affecting the primary dentition and
leadind to tooth exfoliation early in life are usually interpreted
as periodontal manifestation of systemic diseases- leukocyte
adhesion deficiency.

20. PERMANENT DENTITION
 13 to 20 year old individuals, the majority of studies have reported
a prevalence of periodontitis of less than 1 % .
 Among US school children 5-17 years of age, the prevalence of
periodontitis has been estimated to range from about 0.2% for
whites to about 2.6% for blacks (Loe & Brown 1991).
 Blacks were at much higher risk for LAP, and black males were at
2.9 times higher risk.
 White females were more likely to have LAP than white males.
 In a study of untreated periodontal disease conducted by Loe et al.
(1986) in Srilanka, 8% of population had rapid progression of
periodontal disease, characterized by yearly attachment loss of
0.1-1 mm.

21. SCREENING
 Cost effective detection of cases require utilization of a
sensitive screening approach.
 Most sensitive diagnostic test is measurement of
attachment loss by probing.
 In younger subjects, currently utilized method is the
measurement of the distance between alveolar crest and
CEJ on bitewing radiographs.
 Recent investigations have attempted to determine the
‘Normal’ distance between CEJ and alveolar crest of
primary and permanent molars in 7-9 year old children
(Sjodin & Mattson et al 1997).

22.  Median distances at primary molars were 0.8-1.4 mm.
 CEJ of permanent molars was 0-0.5 mm apical to
alveolar crest in 7-9 year olds.
 Most of children present distances significantly
smaller than 2-3 mm considered normal for
completely erupted dentitions of adults.
 A distance of 2 mm between CEJ and alveolar crest,
in absence of local factors (caries, restorations, open
contacts), can be suspected for diagnosis of
periodontitis (Sjoidin & Mattson 1992).
 In older individuals, PERIODONTAL PROBING is a
more appropriate screening method.

23.  CIRCUMFERENTIAL PROBING to be done at all the sites
around the teeth.
 The American Academy of Periodontology has recently
endorsed a simplified screening examination for this purpose.
 This examination is based on a modification of Community
Periodontal Index of Treatment Needs (CPITN) (Ainamo et
al 1982; AAP & ADA 1992)

24. ETIOLOGY AND PATHOGENESIS
Dominant microorganisms in LAP :
 Aggregatibacter actinomycetamcomitans,
Capnocytophaga sp., Eikenella corrodens, Prevotella sp.,
Campylobacter rectus.
 Gram positive isolates : streptococci, peptostreptococci.
 Aggregatibacter actinomycetamcomitans, Capnocytophaga,
Prevotella sp. Are predominant members of subgingival flora.

25. Aggregatibacter actinomycetamcomitans
 Key microorganism in LAP.
 Short, facultatively anaerobic, non-motile, gram
negative rod.
 This view was principally based on four lines of
evidence (Socransky & Haffajee 1992):
1. Aggregatibacter actinomycetamcomitans was isolated
in more than 90% of LAP patients. In some studies, it
was possible to demonstrate elevated levels of A.a in
sites showing evidence of recent or ongoing periodontal
tissue destruction (Haffajee et al 1984; Mandell 1984;
Mandell et al 1987.)

26. 2. Demonstration of virulence factors:
Aggregatibacter actinomycetamcomitans produces
several potentially pathogenic substances, including
leukotoxin and is capable of inducing disease in
experimental animals and non-oral sites. It can
translocate across epithelial membranes. ( Zambon et al
1988, Slots & Schonfeld 1991).
3. Findings of immune response towards this bacterium:
elevated levels of serum antibodies to
Aggregatibacter actinomycetamcomitans in LAP
patients (Listgarten et al 1981, Tsai et al 1981, Altman
et al 1982, Ebersole et al 1982).

27. 4.Clinical studies showing correlation between treatment
outcomes and levels of Aggregatibacter
actinomycetamcomitans after therapy: unsuccessful
treatment outcomes linked to failure in reduction of
subgingival load.
Consequently, highly sensitive tests detect the
bacterium would be useful diagnostic tools.
Several studies, provide evidence of transmission
between humans; DiRienzo et al 1990; Preus et al
1992; Petit et al 1993; Poulsen et al 1994.

28.  Using monoclonal antibody technology, five serotypes
(a,b,c,d,e) of Aggregatibacter actinomycetamcomitans
can be distinguished.
 Serotype b strains often isolated from patients with
localized juvenile periodontitis than from other subjects
(Zambon et al 1983, 1996).
 Several properties of Aggregatibacter
actinomycetamcomitans are regarded as important
determinants of virulence and pathogenic potential.
Leukotoxin
production is considered highly significant since it may
play important role in A.a’s evasion of local host
defences.

29. LEUKOTOXIN: role in evasion of local host defences.
 Belongs to family of RTX (Repeats in ToXin),which are
pore-forming lytic toxins.
 Exhibits cytotoxic specificity and destroys human PMN
leukocytes and macrophages, but neither epithelial and
endothelial cells, nor fibroblasts.
 Serotype-b strain (JP2 Clone) present in high frequency
in patients with LJP. This strain was isolated from African
American child with prepubertal periodontitis (Tsai et al
1984).

30. FACTOR SIGNIFICANCE
LEUKOTOXIN Destroys human PMN leukocytes and macrophages.
ENDOTOXIN Activates host cells to secrete inflammatory mediators
(PGs, IL-1b, TNF-a
BACTERIOCIN May inhibit growth of beneficial species
IMMUNOSUPPRESSI
VE FACTORS
May inhibit IgG and IgM production.
COLLAGENASES
CHEMOTACTIC
INHIBITION
FACTORS
Cause degradation of collagen.
May inhibit neutrophil chemotaxis

31.  Gram negative bacteria consists of lipopolysaccharide (LPS).
 A.a can secrete membrane vesicles that can serve as transport
vehicles to spread endotoxin as well as other pathogenic
substances produced by bacterium.
 LPS can activate host cells & macrophages to secrete
inflammatory mediators such as Prostaglandins, IL-1b,
TNF-a.
 It is highly immunogenic, since high titers of antibodies
against its antigenic determinants are frequently detected in
infected individuals

32. Dominant organisms in GAP
 Porphyromonas gingivalis, Bacteroides forsythus and
A.a.
 A.a is facultative anaerobe; P.gingivalis and B.
forsythus are fastidious strict anaerobes.
 P. gingivalis produce collagenases, proteases,
endotoxins, fatty acids, other possibly toxic agents
(Shah 1993).
 High local and systemic immune responses against this
bacterium have been demonstrated in patients with
GAP.

33. BACTERIAL DAMAGE TO
PERIODONTIUM
Two related mechanisms:
1. Direct action of the microorganism or their products
on the host tissues.
2. Results of the eliciting tissue damaging inflammatory
responses.
Investigations have indicated that A.a is able to
translocate through junctional epithelium and invade
the underlying connective tissue (Saglie et al 1988).

34.  Apical spread of bacteria loosely adhering to hard,
non shedding surface of tooth is thought to be
controlled through first line of defence.
Mechanisms:
 High turnover rate of junctional epithelium
keratinocytes.
 Outward flow of GCF.
 Directed migration of PMN leukocytes through
junctional epithelium.

35. HOST RESPONSE TO BACTERIAL
PATHOGENS
 Local inflammatory response characterized by intense
recruitment of PMNs both within the tissues and into
periodontal pocket.
 Depressed T-helper cell to T-suppressor cell ratio
compared to both healthy gingiva and peripheral blood.
 High levels of PGE2, IL-1a, IL-1b in both crevicular
fluid and peripheral blood.
 Prostaglandin E2 production is highly elevated in AgP
subjects when compared to periodontally healthy
individuals and chronic periodontitis patients.

36. IMMUNOLOGICAL FACTORS
 The human leukocyte antigens (HLAs), which regulate immune
responses, have been evaluated as candidate markers for aggressive
periodontitis.
 HLA A9, B15 antigens are consistently associated with aggressive
periodontitis.
 Patients with aggressive periodontitis display functional defects of
polymorphonuclear leukocytes (PMNs), monocytes, or both.
 These defects can impair either the chemotactic attraction of PMNs to the
site of infection or their ability to phagocytose and kill microorganisms.
 Current studies demonstrate hyper responsiveness of monocytes from
LAP patients involving the production of PGE2 in response to
Lipopolysaccharide.
 This lead to increased connective tissue or bone loss due to excessive
catabolic factors.

37. Possible immune mechanisms include
 Increase in expression of MHC II, HLA DR4.
 Polyclonal activation of B cells by microbial
plaque.
 Genetic predisposition.

38. GENETIC ASPECTS OF HOST
SUSCEPTIBILITY
 SEGREGATION ANALYSIS : autosomal dominant
inheritance.
 Segregation analysis provides information about the mode of
inheritance of a genetic trait but not about the specific gene
involved.
 LINKAGE ANALYSIS: linkage of LAP to Vitamin D
binding locus on region q of chromosome 4 in large family of
Brandywine population (Boughman et al 1986).
 Li et al 2004 : has shown linkage of LAP with q25 region of
chromosome 1.
 Scapoli et al 2005: showed linkage with q13-14 region of
chromosome 2 that contains IL-1 gene complex.

39.  Tonetti and Mombelli,1999 summarized that “it
seems that specific genes may be different in
various populations and/or ethnic groups and
therefore true heterogeneity in disease
susceptibility may be present.
 The role of specific genes remains to be
elucidated”.

40. ENVIRONMENTAL ASPECTS OF HOST
SUSCEPTIBILITY
 Cigarette smoking was shown to be a risk factor for patients
with GAP. (Schenkein et al 1995).
 Smokers with GAP have more affected teeth and greater
means of attachment loss than patients with GAP who did
not smoke.
 The results indicated that IgG2 levels as well as antibody
levels are significantly depressed in subjects with GAP
who smoke.
 Since these antibodies are considered to represent a
protective response against A.a, it is possible that the
depression of IgG2 in smokers may be associated with the
observed increase in disease extent and severity.

41. CLINICAL DIAGNOSIS
A tentative clinical diagnosis is based on following
criteria:
 Absence of significant systemic conditions.
 Rapid attachment loss and bone destruction.
 Familial aggregation of cases.
 Lack of consistency between clinically visible
bacterial deposits and severity of periodontal
breakdown.

42. LAP GAP
 Circumpubertal onset (13-14 to
25 yr old).
 Localized first molar-incisor
presentatio with interproximal
attachment loss on atleast two
permanent teeth, one of which
is first molar and involving no
more than two teeth other than
first molar.
 Less than 30-35 years.
 Generalized interproximal
attachment loss affecting
atleast three permanent teeth
other than first molars and
incisors.
 Pronounced episodic nature
of destruction of attachment
and alveolar bone.

43. RADIOGRAPHIC DIAGNOSIS
Localised
Aggressive
Periodontitis
Generalised
Aggressive
Periodontitis

44. MICROBIOLOGIC DIAGNOSIS
 Knowledge of whether a clinical condition is associated with
A.a and/or P. gingivalis, has an impact on the need to
supplement conventional therapy with antibiotics and choice
of antimicrobial drug.
 Microbiological testing may be postponed until the first
phase is completed.
 Reduction in bacterial load might increase the possibility of
false negative results when an insensitive microbiological test
is used.
 Since A.a and P. gingivalis can be transmitted from patients to
family members, microbial testing of spouses, children or
siblings of AgP patients may be indicated to intercept early
disease in susceptible patients.

45. EVALUATION OF HOST DEFENSES
 Associated with high incidence of phagocyte
functional disturbances, such as depressed
neutrophil chemotaxis and other phagocyte
antibacterial dysfunctions.
 AgP patients present higher levels of PGE2 in
crevicular fluid.
 The findings indicated that these patients respond to
bacterial and inflammatory stimuli with very high
levels of local release of inflammatory mediators.

46.  GAP patients have decreased ability to mount high
titres of specific IgG2 antibodies to A.a.
 These patients exhibit a tendency towards progressive
periodontal destruction leading to tooth loss.
 LAP have better prognosis and donot express this trait.
 Serum antibody titres and avidity of A.a may be useful
in differential diagnosis of GAP and LAP.

47. GENETIC DIAGNOSIS
 Clinical determination of different disease forms in
family should be followed by construction of a
pedigree of the AgP trait.
 Such diagnosis may bring considerable
information regarding the level of risk eventually
shared within the family.
 It helps to establish the need for monitoring
clinically unaffected individuals.

48. PRINCIPLES OF THERAPEUTIC
INTERVENTION
 Treatment should be initiated after completion of
careful diagnosis.
 Successful treatment is considered to be dependent
on early diagnosis, directing therapy towards
elimination or suppression of infecting organisms
and providing an environment conducive to long-
term maintenance.

49.  The prognosis depends on
1. Whether the disease is generalized or localized.
2. Degree of destruction present at the time of
diagnosis.
3. Ability to control future progression.
GAP rarely undergoes spontaneous remission,
whereas
LAP have been known to arrest spontaneously.
This has been referred to as “BURNOUT” OF
THE DISEASE.

50. CONVENTIONAL PERIODONTAL
THERAPY
 Consists of patient education, oral hygiene improvement,
scaling and root planing and regular recall maintenance.
 Teeth with moderate to advanced attachment loss and bone
loss often have a poor prognosis.
 Treatment options for teeth with deep periodontal pockets and
bone loss may be non-surgical or surgical.
 Surgery may be purely resective, regenerative or a
combination.

51. RESECTIVE SURGICAL THERAPY
 Reduces or eliminates pocket depth.
 If a significant height discrepancy exists between periodontal
support of affected teeth and unaffected teeth, the gingival
transition will often result in deep probing pocket depth around
affected tooth.
 It is important to realize the limitations of surgical therapy and to
appreciate the possible risk that surgical therapy may further
compromise teeth that are mobile because of extensive loss
of periodontal support.
 For example, in a patient with severe horizontal bone loss,
surgical resective therapy may result in increased tooth
mobility that is difficult to manage, and a nonsurgical
approach may be indicated. Therefore careful evaluation of
the risks versus the benefits of surgery must be considered on
a case by- case basis.

52. REGENERATIVE PERIODONTAL
THERAPY
 Use of barrier materials, bone grafts, and wound
healing agents.
 Intrabony defects, particularly vertical defects with
multiple osseous walls are often amenable to
regeneration with these techniques.
 Recent advances in regenerative therapy have
advocated the use of enamel matrix derivative
(Emdogain) to aid in regeneration of cementum and
new attachment in periodontal defects.

53. ANTIMICROBIAL THERAPY
SYSTEMIC ADMINISTRATION
 Adjunctive antibiotic treatment frequently results in a more
favorable clinical response than mechanical therapy alone.
 In a systematic review, Herrera et al found that systemic
antimicrobials in conjunction with scaling and root planing offer
benefits over scaling and planing alone in terms of clinical
attachment level, probing pocket depth, and reduced risk of
additional attachment loss.
 Genco et al treated localized aggressive periodontitis patients
with scaling and root planing plus systemic administration
of tetracycline (250 mg four times daily for 14 days every 8
weeks).
18 months after the initiation of therapy.
Bone loss had stopped, and one-third of the defects
demonstrated an increase in bone level, whereas in the control
group, bone loss continued.

54.  Liljenberg and Lindhe treated also treated LAP with
administration of tetracycline (250 mg 4 times daily for 2
weeks), modified widman flaps, and periodic recall visits
every month for 6 months. The lesions healed rapidly and
more completely.
 After 5 years they found that the treatment group continued to
demonstrate
1.resolution of gingival inflammation,
2. gain of clinical attachment,
3. refill of bone in angular defects.
 Systemic antibiotics should only be administered as an
adjunct to mechanical debridement because
IN UNDISTURBED SUBGINGIVAL PLAQUE, THE
TARGET ORGANISMS ARE EFFECTIVELY
PROTECTED FROM ANTIBIOTIC AGENT DUE TO
BIOFILM EFFECT.

55.  Systemic tetracycline (250mg of tetracycline
hydrochloride four times daily for atleast 1
week) should be given in conjunction to local
mechanical debridement.
 Doxycycline 100mg/day may be used instead
of tetracycline.
 Chlorhexidine rinses should be prescribed
and continued for several weeks to enhance
plaque control and facilitate healing.

56.  Antibiotics have been essentially used in two ways
for treatment:
1. In combination with intensive instrumentation
over a short period of time after achievement of
adequate plaque control in pretreatment motivation
period.
2. As a staged approach after completion of initial
therapy.

57. MICROFLORA ANTIBIOTIC OF CHOICE
Gram positive Amoxicillin-clavulanate potassium
Gram negative Clindamycin
Non oral gram negative,
facultative rods, Pseudomonas,
Staphylococci
Ciprofloxacin
Black pigmented bacteria &
spirochaetes
Metronidazole
Prevotella intermedia,
P.gingivalis
Tetracycline
A. actinomycetamcomitans Metronidazole-amoxicillin
Metronidazole-ciprofloxacin
Tetracycline
P.gingivalis Azithromycin

58.  A randomised controlled clinical trial has provided evidence of
a significant benefit arising from treatment approach
(Guerrero et al. 2005):
1. Achievement of adequate supragingival plaque control
(less than 25% sites with detectable plaque).
2. Subgingival instrumentation for 2-day period.
3. An adjunctive systemic antibiotic regime consisting of
metronidazole (500 mg tid for 7 days) combined with
amoxicillin (500 mg, tid for 7 days)

59. LOCAL DELIVERY
 FORMULATED IN FORM OF SOLUTIONS, GELS,
CHIPS, FIBRES .
Advantages:
 Smaller dosages can be administered inside the pocket.
 No side effects of systemic therapy.
 Increased exposure of the target microorganism to high
concentration therefore more therapeutic levels of
medication.

60. FULL MOUTH DISINFECTION
 Described by Quirynen et al.
 Full mouth debridement completed in two
appointments within a 24 hr period.
 In addition to scaling and root planing, the tongue is
brushed with a chlorhexidine gel (1%) for 1
minute, the mouth is rinsed with a chlorhexidine
solution (0.2%) for 2 minutes, and pockets are
irrigated with 1% chlorhexidine solution.

61. HOST MODULATION
 Administration of agents that modulate the host
response.
 Subantimicrobial dose doxycycline (SDD) : help to
prevent the destruction of PDL attachment by
controlling the activation of MMP’s, primarily
collagenase and gelatinase, from both infiltrating cells
and resident cells of periodontium, primarily neutrophils.
 SDD as an adjunct to repeated mechanical debridement
resulted in clinical improvement in patients with
generalized aggressive periodontitis.
 Other agents such as flubriprofen, indomethacin, and
maproxen may reduce inflammatory mediator
production.

62. CONCLUSION
 Aggressive periodontitis comprises a group of rare, often severe,
rapidly progressive forms of periodontitis , characterised by an
early age of onset and tendency for cases to aggregate in the
families.
 Diagnosis of one of these forms requires the absence of systemic
diseases that may severely impair host defences and lead to
premature exfoliation of teeth.
 Optimal plaque control by patient is of paramount importance for
a favourable clinical and microbiological response to therapy.

63. THANK YOU!!!!!!!