Prepubertal and Juvenile Periodontitis

Dr. Leenu Maimanuku

Prepubertal Periodontitis

Prepubertal Periodontitis
Commonly
Down

associated with systemic diseases

syndrome

Papillon-Lefvre

syndrome Neutropenias Chediak-Higashi syndrome Hypophosphatasia Acute and sub-acute leukemia Leukocyte adhesion deficiency
Onset

before 11 yrs of age Can occur in the primary or the mixed dentition It frequently exists after puberty

Papillon-Lefvre Syndrome
Characterised

by:

Hyperkaratotic

skin lesions Severe destruction of the periodontium Calcification of the lamina dura in some cases Cutaneous and periodontal changes usually occur before the age of 4 years. Skin lesions:
Hyperkeratosis
Ichthyosis

of localised areas on palms, soles, knees ad

elbows.

Oral Manifestations

Early inflammatory changes leading to

Bone loss Exfoliation of teeth

Primary teeth lost by 5 6 yrs of age Permanent dentition erupts normally but lost within a few years By 15yrs patients are usually edentulous except for third molars which are lost a few yrs after eruption too

Microscopic changes
Chronic

inflammation of the lateral wall of the

pocket Plasma cells infiltrate predominates Considerable osteoclastic activity Lack of osteoblastic activity Extremely thin cementum

Etiology

Spirochetes found in
the apical portion of the pocket, Adhering to the cementum

Microcolony formation of Mycoplasma Gram ve cocci and rods at the apical border of plaque Inherited disorder follows an autosomal recessive pattern 1-4/million affected

Down Syndrome
Congenital

disease caused by chromosomal abnormality Characterised by mental deficiency and growth retardation Prevalence of periodontal disease is high Plaque and predisposing local factors commonly present but severity exceeds these.

Clinical features
Deep periodontal pockets Plaque accumulation Moderate gingivitis More severe disease in the lower anterior region, with marked recession. Associated with high frenum Disease progresses rapidly Acute necrotising lesions frequently found

Pathophysiology
Two

factors involved:

Reduced

resistance to infections due to poor circulation, especially areas of terminal vascularization Defect in T-cell maturation and in PMNs chemotaxis

Neutropenias
Destructive

generalized periodontal lesions

Chediak-Higashi syndrome
Rare

syndrome Characterised by:

Recurrent

bacterial infections and Rapidly destructive periodontitis

Hypophosphatasia
Rare

skeletal disease Characterised by:

Rickets Poor

cranial bone formation Craneostenosis Premature loss of primary teeth, particularly incisors Low levels of serum alkaline phosphatase Phosphoethanolamine present in serum and urine

Oral findings
Teeth

lost with no clinical evidence of gingival inflammation Reduced cementum formation Premature loss of decidous teeth Appears like localised juvenile periodontitis in adolescents

Acute and Subacute Leukemia

Accompanied

by sever periodontal changes

Leukocyte Adhesion Deficiency

Rare Begins during or immediately after eruption of primary teeth. Extremely acute inflammation Proliferation of gingival tissues Rapid bone destruction Permanent dentition may not be affected Patient has frequent respiratory tract infections and sometimes otitis media

Pathophysiology
Defects

in peripheral blood neutrophils and monocytes Absence of neutrophils in the gingival tissues

Localised Prepubertal Periodontitis

Involves

only a few teeth Minor inflammation Slow bone loss Mild defects in neutrophils or monocytes but not both, are found

Juvenile Periodontitis

Prevalence
Less

the 1% Highest prevalence amongst black males followed by black females, white females and white males Seen between puberty and 20yrs of age

Distribution of Lesions
Localised
First

lesion (Localised Juvenile Periodontitis)

molars and incisors affected Bilaterally symmetric patterns of bone loss seen frequently
Generalized

Juvenile Periodontitis

Localised Juvenile Periodontitis

Possible reasons for limitation of destruction:

1.

Aa evades the host defenses by different mechanisms:

Production of PMN chemotaxis-inhibiting factors Endotoxins Collagenases Leukotoxins etc.

After the initial attack, immune defenses are stimulated to produce opsonising antibodies to enhance phagocytosis of invading bacteria and neutralise destructive factors. Colonization of other sites prevented.

2.

Bacteria antagonistic to Aa may develop, decrease the number of destructive lesions and colonisation sites

Localised Juvenile Periodontitis

3.

4.

Aa may loose its leukotoxin-producing ability for unknown reasons. Progress og disease arrested or retarded Defect in cementum formation may be responsible for the localization of the lesions. Hypoplastic or aplastic cementum has been found

Clinical findings
No clinical inflammation Deep periodontal pockets Small amount of plaque Calculus is rarely present Mobility and drifting to teeth are common initial symptoms Distolabial migration of maxillary incisors with diastema formation common Dentinal hypersensitivity Deep, dull, radiating pain on mastication Periodontial abscess formation Regional lymph node enlargement

Radiographic findings
Vertical

loss of alveolar bone around first molars and incisors

19 yr old female

Juvenile Periodontitis

Clinical course
Rapid

progress Disease continues until treated or tooth extracted or exfoliated

Heredity
Follows

familial pattern Possibly a result of transmission of microorganisms May be an autosomal recessive trait or a X-linked dominant disease