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AGGRESSIVE PERIODONTITIS 
NIDHI 
B.D.S FINAL YEAR
CONTENTS 
 INTRODUCTION 
 HISTORY 
 AGGRESSIVE PERIODONTITIS 
 DIFFERENCE BETWEEN CHRONIC AND AGGRESSIVE 
PERIODONTITIS 
 CLINICAL FEATURES 
 LOCALIZED AGGRESSIVE PERIODONTITIS 
 GENERALIZED AGGRESSIVE PERIODONTITIS 
 DIFFERENCE BETWEEN LAP & GAP 
 RISK FACTORS 
o MICROBIOLOGIC FACTORS 
o IMMUNOLOGIC FACTORS 
o GENETIC FACTORS 
o ENVIRONMENTAL FACTORS 
 CONCLUSION 
 REFERENCES
INTRODUCTION 
 Periodontitis is defined as an inflammatory 
disease of the supporting tissue of the teeth 
caused by specific microorganisms, resulting in 
progressive destruction of the periodontal 
ligament and alveolar bone with pocket 
formation, recession, or both.
HISTORY 
 1923, Gottlieb -- Case of epidemic influenza 
 “Diffuse atrophy of the alveolar bone” 
 Loss of collagen fibers in the periodontal 
ligament 
 Replacement by loose connective tissue 
 Extensive bone resorption, 
 Resulting in a widened periodontal 
ligament space. 
 The gingiva apparently was not involved.
 In 1938 Wannenmacher described incisor-first 
molar involvement and called the disease 
Parodontitis marginalis progressiva. 
 Finally in 1967, Chaput and colleagues and by Butler 
in 1969 introduce the term Juvenile Peridontitis. 
 In 1989 the World Workshop in Clinical 
Periodontics categorized this disease as ‘Localized 
Juvenile Periodontitis’ (LJP) 
 Most recently , it is named as Aggressive 
Periodontitis.
AGGRESSIVE 
PERIODONTITIS 
 Aggressive periodontitis (AgP) comprises a 
group of rare, often severe, rapidly 
progressive forms of periodontitis often 
characterized by an early age of clinical 
manifestation and a distinctive tendency for 
cases to aggregate in families. 
(Clinical Periodontology and Implant Dentistry 
4th edition)
 Aggressive periodontitis describes three of 
the formerly classified as “early-onset 
periodontitis” 
They are: 
 LOCALIZED AGGRESSIVE PERIODONTITIS 
 GENERALIZED AGGRESSIVE PERIODONTITIS 
 RAPIDLY PROGRESSIVE PERIODONTITIS
CHRONIC 
PERIODONTITIS 
AGGRESSIVE 
PERIODONTITIS 
AGE More prevalent in adults 
but may be present in 
children & adolescents 
Circumpubertal onset in 
LAP & under 30 years of 
age in GAP 
RATE OF 
PROGGRESSION 
Slow rate of progression Rapid rate of progression 
with pronounced episodic 
events of attachment and 
bone loss 
MICROBIAL 
AETIOLOGY 
Consist of both aerobic & 
anaerobic gram positive & 
gram negative 
microorganisms 
Key microorganisms are 
Aggregatibacter 
actinomyctemcomitans & 
Prevotella intermedia 
IMMUNOLOGICAL 
AETIOLOGY 
No abnormalities detected Hyper responsive 
macrophage phenotype & 
phocyte abnormalities
CHRONIC PERIODONTIS AGGRESSIVE 
PERIODONTITIS 
DISTRIBUTION Localized when less than 30% 
of sites involved 
Generalized when more than 
30% of sites are affected 
Localized when 1st molar & 
incisors & no more than two 
permanent teeth are 
involved 
Generalized when at least 
3 permanent teeth other 
than 1st molar & incisor are 
involved 
LOCAL FACTORS Presence of local factors 
directly relates to the 
amount of destruction 
present 
Presence of local factors 
does not commensurate 
with the amount of 
destruction present 
FAMILIAL 
AGGREGATION 
Lacks strong evidence of 
correlation between 
particular genes and 
periodontitis 
Evidence of strong familial 
aggregation
FEATURES OF AGGRESSIVE 
PERIODONTITIS 
(by lang et al. in 1999) 
PRIMARY FEATURES 
 Non contributory medical history 
 Rapid attachment loss and bone loss 
 Familial aggregation
SECONDARY FEATURES 
 Amount of microbial deposits does not 
commensurate with the severity of periodontal 
tissue destruction 
 Elevated proportions of aggregatibacter 
actinomycetemcomitans (Aa) 
 Hyper responsive macrophage phenotype with 
exaggerated response to bacterial endotoxin 
 Phagocyte abnormalities
AGGRESSIVE 
PERIODONTITIS 
LOCALIZED AGGRESSIVE 
PERIODONTITIS 
(previously classified as 
Localized Juvenile 
Periodontitis) 
GENERALIZED 
AGGRESSIVE 
PERIODONTITIS 
(previously classified as 
Generalized Juvenile 
Periodontitis)
LOCALIZED AGGRESSIVE 
PERIODONTITIS 
 Clinically, it is characterized as having 
"localized first molar/incisor presentation with 
interproximal attachment loss on at least two 
permanent teeth, one of which is a first molar, 
and involving no more than two teeth other 
than first molars and incisors” .
 Clinical features: 
1. Age of onset at about puberty. 
2. Affects both the sexes 
3. Main characteristic 
feature  affects mainly the 
FIRST MOLARS and INCISORS 
4. Lack of clinical inflammation 
despite the presence of 
deep periodontal pockets.
5. Plaque that is present forms 
thin biofilm on the teeth. 
6. Plaque contains elevated 
levels of : 
Aggregatibacter 
actinomycetem-comitans 
(Serotype b) 
Porphyromonas gingivalis 
(in some pts) 
7. Disease progresses rapidly and Plaque that is 
present forms a thin biofilm on the teeth 
and rarely mineralizes to form calculus
8. The rate of bone loss is 3 to 4 times 
faster than in chronic 
periodontitis. 
9. Robust serum antibody response. to 
infecting agents
 Other Clinical Findings: 
1. Maxillary incisors migrate disto-labially that 
results in diastema formation. 
2. Increasing mobility of the 
affected teeth 
3. Sensitivity of denuded root surfaces to 
thermal and tactile stimuli 
4. Deep, dull radiating pain during mastication. 
5. Periodontal abscess may form. 
6. Regional lymph node enlargement may occur.
Radiographic finding: 
o Classic diagnostic sign  VERTICAL LOSS of 
alveolar bone around the first molars and incisors. 
o Other finding  “Arc-shaped” loss of alveolar bone 
extending from the distal surface of 2nd premolar 
to the mesial surface of the 2nd molar. 
o Bone defects are usually wider than usually seen 
with chronic periodontitis.
Generalized aggressive 
periodontitis 
“Characterized by generalized interproximal 
attachment loss affecting at least three 
permanent teeth other than first molars and 
incisors”
FEATURES 
 Usually affecting persons under 30 years of 
age, but patients may be older. 
 Poor serum antibody response to infecting 
agents. 
 Generalized interproximal attachment loss 
affecting at least three permanent teeth 
other than first molars and incisors. 
 Pronounced episodic nature of the destruction 
of attachment and alveolar bone.
Radiographic features 
 No definitive pattern of distribution. Ranges 
from severe bone loss associated with the 
minimal no. of teeth, to advanced bone loss 
affecting the majority of teeth in the 
dentition. 
 Patients with GAP demonstrate osseous 
destruction of 25% to 60% during a 9 week 
period and other sites show no bone loss.
Localized aggressive 
periodontitis (LAP) 
Generalized aggressive 
periodontitis (GAP) 
AGE OF ONSET Circumpubertal Under 30 yrs of age but 
older patients may be 
affected 
DISTRIBUTION Localized 1st molar or incisor 
presentation with 
interproximal attachment 
loss & not involving more 
than 2 permanent teeth 
Generalized interproximal 
attachment loss affecting at 
least three permanent teeth 
other than 1st molars & 
incisors 
SEVERITY Rapid & severe loss of 
alveolar bone 
Episodic in nature 
AETIOLOGY Predominantly Aa Predominantly P. gingivalis 
IMMUNOLOGICAL 
Robust serum antibody 
RESPONSE 
response to infecting agent 
Poor serum antibody 
response to infecting agent 
PRESENCE OF 
LOCAL FACTORS 
There is minimal amount of 
local factors present on the 
affected teeth 
There is marked plaque & 
calculus accumulation 
FAMILIAL 
PATTERN 
Strong association Unclear association
Localized Aggressive 
Periodontitis 
Generalized Aggressive 
Periodontitis 
GINGIVAL 
INFLAMMATION 
Lack of clinical 
inflammation despite the 
presence of deep pockets 
and advanced bone loss 
Clinical signs of gingival 
inflammation are evident 
RADIOGRAPHIC 
APPEARANCE 
Vertical or arc-shaped 
bone loss around 1st molars 
and incisors 
There is generalized 
extensive destruction or 
bone loss around involved 
teeth
Risk factors for aggressive form of 
periodontitis 
 Microbiologic factors 
 Immunologic factors 
 Genetic factors 
 Environmental factors
Microbiologic factors 
 Presence of Aggregatibacter 
actinomycetemcomitans (Aa) is a key agent in 
LAP as it is present in high nos. & the patient 
has high titre of serum antibodies against Aa. 
 Virulence factors possessed by Aa, such as 
leucotoxin, lipopolysaccharide, proteases, 
collagenases, surface associated material 
affect the immune response & lead to 
connective tissue destruction and bone 
resorption.
Immunologic factors 
 Defective chemotaxis due to functional defect 
of PMNs. 
 Hyper responsive monocytes that increase 
prostaglandin, IL-1 α IL-1βproduction, which 
result in one resorption. 
 Human leucocyte antigen (HLA) A9 & B 15 are 
recognized as candidate markers of aggressive 
periodontitis.
Genetic factors 
 Tendency to occur in families: familial 
aggregation 
 Segregation & linkage analysis have shown that 
presence of specific gene is responsible for 
neutrophil abnormalities 
 Transmission through autosomal- dominant 
mode of inheritance
Environmental factors 
Smoking has a significant influence in the 
progression of generalized aggressive 
periodontitis. Smokers have greater 
attachment loss than non smokers.
CONCLUSION 
 Aggressive forms of periodontitis are currently 
considered to be multifactorial diseases developing as a 
result of complex interactions between specific host 
genes and the environment. 
 Interactions between the disease process and 
environmental factors and genetically controlled 
modifying factors are thought to contribute to 
determining the specific clinical manifestation of the 
disease. 
 For a successful treatment outcome the conventional 
therapy is to be combined with a wide range of 
therapeutic procedures to increase the chances of 
disease resolution.
REFERENCES 
 CARRANZA’S CLINICAL PERIODONTOLOGY; 
10th edition. 
 J LINDHE; CLINICAL PERIODONTOLOGY 
AND IMPLANT DENTISTRY: 4th edition
Aggresive periodontitis

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Aggresive periodontitis

  • 2. CONTENTS  INTRODUCTION  HISTORY  AGGRESSIVE PERIODONTITIS  DIFFERENCE BETWEEN CHRONIC AND AGGRESSIVE PERIODONTITIS  CLINICAL FEATURES  LOCALIZED AGGRESSIVE PERIODONTITIS  GENERALIZED AGGRESSIVE PERIODONTITIS  DIFFERENCE BETWEEN LAP & GAP  RISK FACTORS o MICROBIOLOGIC FACTORS o IMMUNOLOGIC FACTORS o GENETIC FACTORS o ENVIRONMENTAL FACTORS  CONCLUSION  REFERENCES
  • 3. INTRODUCTION  Periodontitis is defined as an inflammatory disease of the supporting tissue of the teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both.
  • 4. HISTORY  1923, Gottlieb -- Case of epidemic influenza  “Diffuse atrophy of the alveolar bone”  Loss of collagen fibers in the periodontal ligament  Replacement by loose connective tissue  Extensive bone resorption,  Resulting in a widened periodontal ligament space.  The gingiva apparently was not involved.
  • 5.  In 1938 Wannenmacher described incisor-first molar involvement and called the disease Parodontitis marginalis progressiva.  Finally in 1967, Chaput and colleagues and by Butler in 1969 introduce the term Juvenile Peridontitis.  In 1989 the World Workshop in Clinical Periodontics categorized this disease as ‘Localized Juvenile Periodontitis’ (LJP)  Most recently , it is named as Aggressive Periodontitis.
  • 6. AGGRESSIVE PERIODONTITIS  Aggressive periodontitis (AgP) comprises a group of rare, often severe, rapidly progressive forms of periodontitis often characterized by an early age of clinical manifestation and a distinctive tendency for cases to aggregate in families. (Clinical Periodontology and Implant Dentistry 4th edition)
  • 7.  Aggressive periodontitis describes three of the formerly classified as “early-onset periodontitis” They are:  LOCALIZED AGGRESSIVE PERIODONTITIS  GENERALIZED AGGRESSIVE PERIODONTITIS  RAPIDLY PROGRESSIVE PERIODONTITIS
  • 8. CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS AGE More prevalent in adults but may be present in children & adolescents Circumpubertal onset in LAP & under 30 years of age in GAP RATE OF PROGGRESSION Slow rate of progression Rapid rate of progression with pronounced episodic events of attachment and bone loss MICROBIAL AETIOLOGY Consist of both aerobic & anaerobic gram positive & gram negative microorganisms Key microorganisms are Aggregatibacter actinomyctemcomitans & Prevotella intermedia IMMUNOLOGICAL AETIOLOGY No abnormalities detected Hyper responsive macrophage phenotype & phocyte abnormalities
  • 9. CHRONIC PERIODONTIS AGGRESSIVE PERIODONTITIS DISTRIBUTION Localized when less than 30% of sites involved Generalized when more than 30% of sites are affected Localized when 1st molar & incisors & no more than two permanent teeth are involved Generalized when at least 3 permanent teeth other than 1st molar & incisor are involved LOCAL FACTORS Presence of local factors directly relates to the amount of destruction present Presence of local factors does not commensurate with the amount of destruction present FAMILIAL AGGREGATION Lacks strong evidence of correlation between particular genes and periodontitis Evidence of strong familial aggregation
  • 10. FEATURES OF AGGRESSIVE PERIODONTITIS (by lang et al. in 1999) PRIMARY FEATURES  Non contributory medical history  Rapid attachment loss and bone loss  Familial aggregation
  • 11. SECONDARY FEATURES  Amount of microbial deposits does not commensurate with the severity of periodontal tissue destruction  Elevated proportions of aggregatibacter actinomycetemcomitans (Aa)  Hyper responsive macrophage phenotype with exaggerated response to bacterial endotoxin  Phagocyte abnormalities
  • 12. AGGRESSIVE PERIODONTITIS LOCALIZED AGGRESSIVE PERIODONTITIS (previously classified as Localized Juvenile Periodontitis) GENERALIZED AGGRESSIVE PERIODONTITIS (previously classified as Generalized Juvenile Periodontitis)
  • 13. LOCALIZED AGGRESSIVE PERIODONTITIS  Clinically, it is characterized as having "localized first molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors” .
  • 14.  Clinical features: 1. Age of onset at about puberty. 2. Affects both the sexes 3. Main characteristic feature  affects mainly the FIRST MOLARS and INCISORS 4. Lack of clinical inflammation despite the presence of deep periodontal pockets.
  • 15. 5. Plaque that is present forms thin biofilm on the teeth. 6. Plaque contains elevated levels of : Aggregatibacter actinomycetem-comitans (Serotype b) Porphyromonas gingivalis (in some pts) 7. Disease progresses rapidly and Plaque that is present forms a thin biofilm on the teeth and rarely mineralizes to form calculus
  • 16. 8. The rate of bone loss is 3 to 4 times faster than in chronic periodontitis. 9. Robust serum antibody response. to infecting agents
  • 17.  Other Clinical Findings: 1. Maxillary incisors migrate disto-labially that results in diastema formation. 2. Increasing mobility of the affected teeth 3. Sensitivity of denuded root surfaces to thermal and tactile stimuli 4. Deep, dull radiating pain during mastication. 5. Periodontal abscess may form. 6. Regional lymph node enlargement may occur.
  • 18. Radiographic finding: o Classic diagnostic sign  VERTICAL LOSS of alveolar bone around the first molars and incisors. o Other finding  “Arc-shaped” loss of alveolar bone extending from the distal surface of 2nd premolar to the mesial surface of the 2nd molar. o Bone defects are usually wider than usually seen with chronic periodontitis.
  • 19. Generalized aggressive periodontitis “Characterized by generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors”
  • 20. FEATURES  Usually affecting persons under 30 years of age, but patients may be older.  Poor serum antibody response to infecting agents.  Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors.  Pronounced episodic nature of the destruction of attachment and alveolar bone.
  • 21. Radiographic features  No definitive pattern of distribution. Ranges from severe bone loss associated with the minimal no. of teeth, to advanced bone loss affecting the majority of teeth in the dentition.  Patients with GAP demonstrate osseous destruction of 25% to 60% during a 9 week period and other sites show no bone loss.
  • 22. Localized aggressive periodontitis (LAP) Generalized aggressive periodontitis (GAP) AGE OF ONSET Circumpubertal Under 30 yrs of age but older patients may be affected DISTRIBUTION Localized 1st molar or incisor presentation with interproximal attachment loss & not involving more than 2 permanent teeth Generalized interproximal attachment loss affecting at least three permanent teeth other than 1st molars & incisors SEVERITY Rapid & severe loss of alveolar bone Episodic in nature AETIOLOGY Predominantly Aa Predominantly P. gingivalis IMMUNOLOGICAL Robust serum antibody RESPONSE response to infecting agent Poor serum antibody response to infecting agent PRESENCE OF LOCAL FACTORS There is minimal amount of local factors present on the affected teeth There is marked plaque & calculus accumulation FAMILIAL PATTERN Strong association Unclear association
  • 23. Localized Aggressive Periodontitis Generalized Aggressive Periodontitis GINGIVAL INFLAMMATION Lack of clinical inflammation despite the presence of deep pockets and advanced bone loss Clinical signs of gingival inflammation are evident RADIOGRAPHIC APPEARANCE Vertical or arc-shaped bone loss around 1st molars and incisors There is generalized extensive destruction or bone loss around involved teeth
  • 24. Risk factors for aggressive form of periodontitis  Microbiologic factors  Immunologic factors  Genetic factors  Environmental factors
  • 25. Microbiologic factors  Presence of Aggregatibacter actinomycetemcomitans (Aa) is a key agent in LAP as it is present in high nos. & the patient has high titre of serum antibodies against Aa.  Virulence factors possessed by Aa, such as leucotoxin, lipopolysaccharide, proteases, collagenases, surface associated material affect the immune response & lead to connective tissue destruction and bone resorption.
  • 26. Immunologic factors  Defective chemotaxis due to functional defect of PMNs.  Hyper responsive monocytes that increase prostaglandin, IL-1 α IL-1βproduction, which result in one resorption.  Human leucocyte antigen (HLA) A9 & B 15 are recognized as candidate markers of aggressive periodontitis.
  • 27. Genetic factors  Tendency to occur in families: familial aggregation  Segregation & linkage analysis have shown that presence of specific gene is responsible for neutrophil abnormalities  Transmission through autosomal- dominant mode of inheritance
  • 28. Environmental factors Smoking has a significant influence in the progression of generalized aggressive periodontitis. Smokers have greater attachment loss than non smokers.
  • 29. CONCLUSION  Aggressive forms of periodontitis are currently considered to be multifactorial diseases developing as a result of complex interactions between specific host genes and the environment.  Interactions between the disease process and environmental factors and genetically controlled modifying factors are thought to contribute to determining the specific clinical manifestation of the disease.  For a successful treatment outcome the conventional therapy is to be combined with a wide range of therapeutic procedures to increase the chances of disease resolution.
  • 30. REFERENCES  CARRANZA’S CLINICAL PERIODONTOLOGY; 10th edition.  J LINDHE; CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY: 4th edition