Pre Pubertal and Juvenile Period on Tit Is

8/4/2019 Pre Pubertal and Juvenile Period on Tit Is

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Prepubertal and Juvenile

Periodontitis

Dr. Leenu Maimanuku


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Prepubertal Periodontitis


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Prepubertal PeriodontitisCommonly associated with systemic diseasesPapillon-Lefvre syndrome

Down syndrome

NeutropeniasChediak-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


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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.


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Oral Manifestations Early inflammatory changes leading to

Bone loss

Exfoliation of teeth

Primary teeth lost by 56 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


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Microscopic changesChronic inflammation of the lateral wall of the

pocket

Plasma cells infiltrate predominates

Considerable osteoclastic activity

Lack of osteoblastic activityExtremely thin cementum


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Etiology Spirochetes found in

the apical portion of the pocket,

Adhering to the cementum

Microcolony formation of Mycoplasma

Gramve cocci and rods at the apical border of plaque

Inherited disorderfollows an autosomal recessive pattern

1-4/million affected


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Down SyndromeCongenital 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.


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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


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PathophysiologyTwo factors involved:

Reduced resistance to infections due to poor

circulation, especially areas of terminal vascularization

Defect in T-cell maturation and in PMNs chemotaxis


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NeutropeniasDestructive generalized periodontal lesions


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Chediak-Higashi syndromeRare syndrome

Characterised by:

Recurrent bacterial infections and

Rapidly destructive periodontitis


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HypophosphatasiaRare skeletal disease

Characterised by:

Rickets

Poor cranial bone formation

Craneostenosis

Premature loss of primary teeth, particularly incisorsLow levels of serum alkaline phosphatase

Phosphoethanolamine present in serum and urine


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Oral findingsTeeth lost with no clinical evidence of gingival

inflammation

Reduced cementum formation

Premature loss of decidous teeth

Appears like localised juvenile periodontitis inadolescents


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Acute and Subacute LeukemiaAccompanied by sever periodontal changes


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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 andsometimes otitis media


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PathophysiologyDefects in peripheral blood neutrophils and

monocytes

Absence of neutrophils in the gingival tissues


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Localised Prepubertal Periodontitis Involves only a few teeth

Minor inflammation

Slow bone loss

Mild defects in neutrophils or monocytes but not

both, are found


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Juvenile Periodontitis


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PrevalenceLess the 1%

Highest prevalence amongst black males followed

by black females, white females and white males

Seen between puberty and 20yrs of age


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Distribution of LesionsLocalised lesion (Localised Juvenile Periodontitis)

First molars and incisors affected

Bilaterally symmetric patterns of bone loss seen

frequently

Generalized Juvenile Periodontitis


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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 ofinvading 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


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Localised Juvenile Periodontitis

3. Aa may loose its leukotoxin-producing ability for

unknown reasons. Progress og disease arrested or

retarded

4. Defect in cementum formation may be

responsible for the localization of the lesions.

Hypoplastic or aplastic cementum has beenfound


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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

Re ional l m h node enlar ement


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Radiographic findingsVertical loss of alveolar bone around first molars

and incisors


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19 yr old female


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Juvenile Periodontitis


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Clinical courseRapid progress

Disease continues until treated or tooth extracted

or exfoliated


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Heredity Follows familial pattern

Possibly a result of transmission of

microorganisms

May be an autosomal recessive trait or a X-linked

dominant disease

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Pre Pubertal and Juvenile Period on Tit Is