Juvenile periodontitis

Almost covers all the information regarding localized & generalized aggressive/juvenile periodontitis

2. :Contents:
Introduction
Classification
Localized Juvenile Periodontitis:
Etiology
Clinical Features
Radiographic Features
Generalized Juvenile Periodontitis
Etiology
Clinical Features
Radiographic Features
Microbiology
Immunology
Differential Diagnosis
Treatment
Conclusion
References

3. PERIODONTIUM:
The normal healthy periodontium consists of
several tissues namely:
1. Gingiva ,
2. Periodontal ligaments(PDL) ,

3. Cementum ,
4. Alveolar bone
For the maintenance of the tooth in the oral
cavity, the health of the periodontium as a whole is
of paramount importance.

4. Cementum
Gingiva

5. Early onset Periodontitis,
Aggressive Periodontitis
INTRODUCTION:
 Juvenile Periodontitis is the most
uncommon severe form of the Periodontal disease

 Described by Wannenmacher(1938) as
destruction of the supporting tissues of the teeth
that becomes clinically significant during
adolescence or early adulthood.

8. CLASSIFICATION:
Ranney,1993,classified the disease in Localized &
Generalized form
1.Localized aggressive periodontitis:
- Characterized by bone loss around the first
molars & incisors
- Occurring in otherwise healthy individuals
2.Generalized aggressive periodontitis:
- Characterized by a more widespread
pattern of periodontal destruction
- Associated with a variety of diseases of
other systems

10. 1.LOCALIZED JUVENILE PERIODONTITIS
ETIOLOGY:-
• Actinobacillus actinomycetemcomitans are
the most commonly found bacteria at the
diseased sites .
•Other micro-organisms found are:
P. gingivalis, E.corrodens, Capnocytophaga,
Spirochetes ,Bacillus,etc.
•Elevated levels of A.a. found in active sites
(low in numbers at healthy sites)

11. •Produce leukotoxins, collagenase,bone
resorbing factors & other
immunosuppressive factors that help in
invasion of host tissues,evasion of host
defences leading to the destruction of
periodontal tissue.
•Incidence of A.a. found to be greater in
younger persons compared to older clients
•Younger patients experience more
destruction in a shorter period of time

13. CLINICAL FEATURES:-
Onset around the time of puberty .
 Occur in an otherwise healthy individual,
clinical inflammation may not be obvious.
 Localized almost exclusively to the incisors & first
molars, less than 30% of sites are involved.

 Females are affected more than males
 Blacks affected more than whites
 Abnormality in the phagocyte function .
 Self arresting disease progression.

14.  Earliest Sign Drifting of teeth in a patient
having a good oral hygiene
Affected teeth becomes mobile followed by pocket
formation.
 Progression of bone loss is 3-5 times faster than
adult periodontitis.
 Maxillary incisors migrate in distolabial
direction  diastema.
 Sensitive root surfaces
 Deep,dull,radiating pain may occur with
mastication (irritation of the supporting tissues)
 Periodontal abscess formation

17. Diastema

18. Denuded root surface

20. Some reasons why disease activity
affects certain teeth:
 A.a. colonize first perm. teeth to erupt
- Evade host defenses
- Following initial attack, host responds
- Antibodies produce which improve phagocytosis
of bacteria
- This may prevent colonization at other sites
 A.a. may lose its ability to produce
leukotoxin
- This may slow or arrest the disease process

21.  Antagonistic bacteria
- Anti-A.a. bacteria may colonize sites &
prevent A.a. from colonizing other sites in
mouth
- Localizes the infection & tissue destruction
 Denuded root surfaces
- The root surfaces of patients with LJP are
often denuded (absence of cementum)
- Allows bacteria to penetrate the root and
colonize the site

22. RADIOGRAPHIC FEATURES:
1.A localized vertical bone loss with widening of
PDL space
2. Arc shaped bone destruction starting from the
distal margin of the second premolar & extending
to the mesial margin of the second molar

24. 2. GENERALIZED JUVENILE PERIODONTITIS
ETIOLOGY:
• Actinobacillus actinomycetemcomitans along
with the diverse microbiota.
• Defective neutrophil or monocyte function.
• Poor serum antibody response to infecting agent
is seen.
• Subgingival tissues shows the presence of gram
negative rods including P.Gingivalis & exhibit
suppressed neutrophil chemotaxis.

26. CLINICAL FEATURES:

Usually affect an individual under 30 years of age
 Generalized involvement of permanent teeth, more than 30
percent.
 Affects atleast 3 permanent teeth other than first molar &
incisors
 The destruction often appears episodically, with periods of
advanced destruction followed by stages of quiescence of
variable length.
 Patients often have small amounts of bacterial plaque
associated with the affected teeth.
 Destructive phase:
Tissue appears severely inflamed, ulcerated & fiery red
Bleeding with or without stimulation
Suppuration
Attachment & bone loss usually occurs

27. Non-destructive phase:
Tissues appear pink with some stippling
Lack of inflammation
Probing will reveal deep pockets
Bone & attachment levels relatively stable
Some patients with GAP may exhibit:
Weight loss,
Mental depression,
General malaise.

Systemic conditions may predispose patient to GAP, these
include:
Chronic neutrophil defects,
leukocyte adherence deficiency,etc.

29. Destructive
phase
Non destructive
phase

30. Pus formation

32. RADIOGRAPHIC FEATURES:
1.Severe bone loss associated with minimal no. of
teeth to advanced bone loss affecting the majority
of the teeth

36. MICROBIOLOGY:
Actinobacillus actinomycetemcomitans
appears to be primarily associated with the disease.

- Gram negative anaerobes
- Rod shaped organisms
- Localized predominantly at the base of the defect

The presence of a recently discovered genus
termed Capnocytophaga, has been associated with the
progression of periodontitis lesions.

37. IMMUNOLOGY:
Defective function or production of
circulating neutrophils & monocytes is often
associated with an increased frequency & severity of
bacterial infection.
DIFFERENTIAL DIAGNOSIS:
Conditions that could contribute to alveolar
bone loss in the primary dentition & premature loss
of primary teeth:
1. Hypophosphatasia
2. Papillon – Lefevre syndome
3. Cyclic Neutropenia

39. HYPOPHOSPHATASIA :

40. TREATMENT:
1.Early diagnosis aids in successful treatment.
2.Extraction of involved teeth (depends on severity of tissue loss)
3.Antibiotics can be provided against infective microorganisms:
Tetracycline is consider the drug of choice
(1g/day orally for 14 days )
Tetracycline+Metronidazole
Doxycycline
4. Periodontal therapy:
 Scaling & root planning
Plaque control instruction
Debridement with or without flap surgery
Subgingival Irrigation with iodine & hydrogen
peroxide
Bone grafts, root resections, hemi sections

41. CONCLUSION:
Periodontal Disease accounts for a
majority of missing teeth in adults & results in
tremendous economic & social burdens both to the
individual & the society.
Periodontal disease is so prevalent
that only possible solution to the problem is its
“prevention” by maintaining the good oral
hygiene.

42. REFERENCES:
1.Essential of Pediatric Oral Pathology  By Mayur
Chaudhary, Sweta Dixit Chaudhary
2.Textbook of Pedodontics  By Shobha Tandon
3.Textbook of Oral Pathology  By Shafer’s
4.Principle & practice of Pedodontics  By Aarthi Rao