This document discusses soft tissue oral lesions in children. It covers drug-induced gingival hyperplasia caused by phenytoin, which causes painless enlargement of the gums. Conditioned enlargements related to puberty can also occur due to hormonal changes. Nutritional deficiencies like scurvy from a lack of vitamin C can result in bleeding gums. Non-specific enlargements like granuloma pyogenicum present as tumor-like masses. Allergic reactions from drugs may also manifest as gingival inflammation. Juvenile periodontitis is an early-onset aggressive form of the disease typically affecting teens. Papillon-Lefevre syndrome is a rare condition characterized by palm and sole

1. SOFT TISSUE ORAL
LESIONS IN CHILDREN
Chinthamani Laser Dental Clinic

2. Drug induced gingival
hyperplasia (PIGO)
Also known as phenytoin induced gingival
overgrowth.

Dilantin hyperplasia.
ETIOLOGY: Multifactorial
a)
Disturbance in adrenocortical function
b)
Local response to metabolic products of phenytoin in
saliva
c)
Direct action on phenytoin on fibroblast.

It is related to the efficacy of oral hygiene and, thus
to the amount of plaque, and inadequate amounts of
antimicrobial factors in the oral cavity could
contribute to greater plaque accumulation.


3. Clinical features

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Appears as early as 2 to 3 weeks after initiation of
drug therapy, peaks at 18 to 24 months.
Painless enlargement of interproximal gingiva.
The buccal & anterior segment are more affected than
the lingual & posterior segments.
Gingiva appears pink and firm
Does not bleed on probing.
Lesion is purely fibrotic in nature or…
Secondary infection superimposes and combined type
of inflammatory enlargement ensues.

4. Clinical features


As interdental
lobulations grow,
clefting becomes
apparent at the midline
of tooth.
Lobulations coalesce at
the midline forming
pseudopockets and
covering most of crown
tooth

5. TREATMENT
Symptomatic treatment:
-Antihistamines
-Topical steroids
-Folic acid
-Ascorbic acid
-Topical antibiotics
-Alkaline mouth washes
 Vigorous gingival massage coupled with efficient
tooth brushing and gum stimulators.


6. Treatment
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Surgical approach:
Gingivectomy with
periodontal knives.
Laser
Electrosurgery
Internal bevel flap
surgery

7. CONDITIONED ENLARGEMENTS
Occurs when the systemic condition of the
patient exaggerates or distorts the normal
response to the dental plaque.
 Includes:
Pubertal gingivitis
Non-specific
Nutritional
Allergic


8. Hormonal (pubertal gingivitis)
ETIOLOGY:
 Hormonal changes



Direct effect on perio. tissue metabolism
Permeability of the vascular system
Microbiota react specifically to availability of
hormones in oral fluids.

9. Clinical features
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Circumpubertal enlargement
Sex: both in males and females
Appears in areas of local irritation
Size of gingival enlargements far exceeds that
usually seen in comparable local factors.
After puberty, the enlargement undergoes a
spontaneous reduction.. But does not disappear
until local factors are removed.

10. Treatment

Removing sources of irritation

Scaling

Curettage

Surgical removal in severe cases

11. NUTRITIONAL(SCURVY)
ETIOLOGY
 Deficiency of
vitamin c

12. Clinical features
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Gingiva :
-bluish red
-soft and friable
-smooth shiny surface
Spontaneous hemorrhage
on slight provocation
Surface necrosis with
pseudomembrane
formation
Enlarged tissue cover the
clinical crown
Typical foul breath with
fusospirochetal stomatitis
Superinfection leading to
ulceration and necrosis of
papillae

13. Treatment

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Ingestion of vit. C
tablets
Diet rich in citrus
fruits
Oral prophylaxis
Maintainence of good
oral hygiene

14. Non specific enlargements
(granuloma pyogenicum)
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The lesion varies from a
discrete spherical ,
tumour like mass with a
pendulated attachment to
a flattened , keliod like
enlargement with a broad
base.
Bright red ,
Either friable or firm,
surface ulceration
Purulent exudation

15. Treatment


Removal of lesion
Eliminating irritating local factors

16. Allergic (plasma cell gingivitis)


The use of drugs may
evoke an allergic
rasponse manifested as
an inflammatory
reaction.
May be associated with
generalised allergic
response.

The gingival and buccal
mucosa on the left side
show pronounced erythema
and slight swelling. Diffuse
ulcerations can also be seen.

17. The inflammatory infiltrate is composed predominately of
plasma cells (He x 400).

18. Treatment

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Stoppage of drugs generally reverses this
condition.
Anti – allergic drugs are of help.

19. Juvenile periodontitis
Uncommon form of severe periodontal disease
belonging to a group termed as an
 EARLY ONSET AGGRESSIVE PERIODONTAL
DISEASE.
 Described by Wannenmacher(1938)
 Age: teenagers
 3 types of disease:
a) chronic slowly progressive
b) fairly generalized
c) acute progressive and more general


20. Etiology
PMN dysfunction
Susceptibility to infection
A. Actinomycetemcomitans
Serum amplification leukotoxin
antibody
neutralisation
Local PMN & macrophage destruction
Accelerated disease

21. Clinical features
Loss of attachment
Bone loss(3-4 times)
Mobility of teeth
Denuded root surface
Periodontal abscess

22. Clinical features (cont.)
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Teeth involved: permanent incisors and first molars.
The attack sequence appear to follow eruption
chronology.
Most striking feature : Lack of clinical inflammation
despite the presence of deep pockets.
Starts as a localized form
if not treated
generalized form

23. Clinical features (cont.)
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Advanced bone loss in the primary dentition
does exit but without destinctive localization.
Every third case presents with
lymphadenopathy
Clinically only thin layer of plaque is present
Classically, distolabial migration of the
maxillary incisors
Diastema formation

24. Radiographic findings
•A full mouth series of
radiographs would be
beneficial in this case
rather than routine bite
wing x-rays.
• Bilateral bone loss is
discovered around all
first molars and incisors.
• Vertical bony defects
are Characteristic in
LJP.

25. Treatment
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Root resection
Subgingival irrigation
with iodine and hydrogen
peroxide.
Scalling and root planing
Tetracycline is antibiotic
of choice
Oral hygiene
maintainence
Bone grafting

26. Preoperative and post operative

27. Papillon lefevre syndrome
Described by : Papillon and Lefevre

Characterized by hyperkeratosis of palms and soles +
precocious periodontal destruction and shedding of the
deciduous and permanent dentition.
ETIOLOGY:

Suggested to be due to
1.
Defective local vitamin A metabolism
2.
Deep subgingival flora assocaited with PLS is composed of
great no. of motile, gram –ve anaerobic rods , including
bacteroids gingivalis and capnocytophagia.
3.
Cellular immune defect with a decreased stimulation of
lymphocytes.
4.
Now generally accepted as the homozygosity of autosomal
recessive genes.


28. Clinical features
a)

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Skin lesions: start b/w
first and fourth year
after birth.
Hyperkeratotic lesions
of palms and soles
bilaterally.
Hyperkeratosis is
usually progressive
and becomes dry and
scaly.

29. Clinical features
b)
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Dental signs and
symptoms:
Swollen gingiva,
migration and mobility of
teeth
Pockets
Fetor-ex-oris
Painless exfoliation
By 3.5 to 4.5 years all the
deciduous teeth are lost.
Eruption of permanent
enhanced
Disease progress recycles
& by ages 13-14 & all
permanent teeth

30. Radiographic findings
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Severe horizontal
alveolar bone loss.
Alveolar bone and basal
bone resorbs beyond
apices of roots.
Incomplete root
resorption.

31. Treatment


Vitamin C metabolites (retinoids):are involved
in regulation of growth and differentiation of
the epithelial cells. Profound effect on
keratinization by dec. the total keratin content
of the keratinocytes.
Antbiotics

32. Email.id:chinthamanidental@gmail.com
044-43800059 , 92 83 786 776
www.chinthamanilaserdentalclinic.com