Pedodontics III Al Azhar University Palestine Gaza Upload By: Lama El Banna lama1997bana@gmail.com Faculty of oral and dental medicine

1. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
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2. College of Dentistry
Pedodontic III
Gingival and Periodontal Problems in
Children -2-
Dr. Hazem El Ajrami
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3. 5. Acute Necrotizing Ulcerative
Gingivostomatitis (ANUG):
 Etiology:
Borrelia vincenti & bacillus fusiformis.
 Duration:
1) Disease is not self limiting.
2) In neglected malnourished children, the
intraoral necrotic process may spread
extensively extraorally (noma or
cancrumoris).
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4. Age:
In developed countries acute necrotizing
ulcerative gingivitis is primarily limited to
adolescents.
In the less developed nations, it also does
affect younger children.
The disease is seen in 18 month children.
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5. Contagious or not:
Not contagious.
Systemic findings:
In severe cases, anorexia, general malaise
& fever may be present.
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6. Oral findings:
Characterized by a rapid destruction of the
interdental papillae associated with pain and
bleeding. A pseudomembrane develops at the
gingival margin as a result of necrosis.
Characteristic foul odour, excessive salivation
and submaxillary lymphadenitis may occur in
severe cases. The involved interdental papillae
appear punched out with an erythematous line
below the necrosed tissue. The degree of tissue
destruction varies and is usually correlated to
some local causative factor (e.g. an open cavity, a
loose primary tooth, poor filling etc.)6

7.  Treatment:
 Local therapy:
1) Removal of local irritating factors.
2) Debridement of the necrotic portion of the
tissues.
3) Swabbing with 3% hydrogen peroxide &
home use of H2O2 (3%).
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8.  Systemic antibiotics:
1) Whether or not to use antibiotics
systemically is a clinical judgment to be
made by the therapist.
2) Systemic antibiotics are recommended only
when massive necrosis has occurred or when
there are systemic effects as fever or
prominent regional lymphadenitis. The fuso-
spirochetal complex is sensitive to penicillin.
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9. 3) Topical utilization of antibiotics is
contraindicated.
4) The use of mild oxidizing mouth rinse after
meals may help in removal of debris and
necrotic material mechanically.
5) Surgical correction of the resulting gingival
deformities may be needed after the relief of
the acute symptoms.
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10. Recurrence:
A difficult in coping with this disease is the
frequency of recurrence.
This recurrence may be the result of:
an immunological phenomena.
persistent gingival deformity.
failure to eliminate local factors.
after cessation of the acute symptoms, the
patient may not return for definitive
treatment.
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11. 6. Recurrent Aphthous Stomatitis:
 Etiology:
1) Unknown, but is frequently associated
with trauma or psychic stress.
2) On occlusion with the intake of certain
foods.
3) Recent investigations suggested a delayed
type of hypersensitivity to certain
microorganisms
4) An autoimmune phenomena may be
involved in the cause.
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12. Duration:
Healing occurs without scaring in 10 to 14
days. Prodromal symptoms of burning and
tingling sensation may be experienced by the
patient 24 to 48 hours preceding the clinical
ulceration.
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13.  Oral findings:
1) The ulcers may vary in number from one to
several dozen.
2) The lesions begin as small localized
erosions of the oral epithelium & are not
preceded by vesicles. Within 2 to 3 days the
ulceration increases in size to reach a
diameter of 1 to 10 mm.
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14. 3) The center of the lesion is grayish and the
sharply delineated margins may or may not be
inflamed.
4) Pain & discomfort are striking clinical
features.
5) Burning and tingling sensation may be
experienced by the patient 24 to 48 hours
preceding the clinical ulceration.
6) Healing occurs without scaring in 10 to 14
days.
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15.  Treatment:
No permanent cure is known. Mild cases
require no treatment. In severe cases,
following symptomatic treatment is
recommended:
1) Surface anesthetic ointment, applied 4 to 5
times daily.
2) Oral achromycin, 250 mg suspension used
as mouth rinse for 1 minute 4 times daily
after meals.
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16. 7. Acute Oral Moniliasis (Candidiasis or
Thrush):
 Etiology:
1) Monilia albicans is a common inhabitant
of the oral cavity but may multiply
rapidly & cause a pathologic state when:
A.Tissue resistance is lowered.
B.The equilibrium between oral
microorganisms is altered.
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17. 2) Prolonged broad spectrum antibiotic therapy
specially topical oral use depresses the coccal
forms of oral flora & in some stimulates the
growth of the yeast (fungi).
3) Moniliasis is found chiefly in premature,
debilitated or malnourished children.
4) It is also more common in institutions where
there is crowding.
5) Mothers with monilial vaginitis may transmit
the infection to the newborn.
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18.  Oral findings:
1) In infants, The lesion consists of an
elevated pearly white or bluish white
adherent patches (superficial growth of the
organisms) on the oral mucosa, at times
extending to the circumoral mucosa.
2) These oral plaques are relatively
nonpainful, removed with difficulty,
leaving a row, painful bleeding surface.
3) Any mucosal surface in the mouth may be
involved.
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19.  Treatment:
1) The topical or systemic antibiotic should be
stopped.
2) A suspension containing 100,000 u/ml of
mycostatin (nystatin) has been found
effective.
3) The administration of 100,000 to 200,000
units of the suspension 3-5 times a day is
effective.
4) To use this drug locally, small amounts (1 ml)
of the suspension should be held in the mouth
several times a day.19

20. 8. Acute Bacterial Gingivitis:
Very rare.
 Diagnosis:
Difficult without extensive laboratory tests.
 Clinical Appearance:
In acute streptococcal gingivitis the gingiva
is bright red, painful, & bleeds easily.
 Treatment:
Broad spectrum antibiotics should be
prescribed if the infection is thought to be
bacterial in origin.
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21. II. Chronic Gingivitis in Children:
This is a mild variety of periodontal
disease which is usually associated with poor
oral hygiene. In chronic gingivitis, the
papillary and marginal gingiva is inflamed.
The condition is reversible and can be treated
by the establishment and maintenance of
good oral hygiene, oral prophylaxis, removal
of calculus deposits and teaching a good tooth
brushing technique.
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22. • As advanced stage of gingivitis commonly seen
in the pre-teen age period is often referred to as
"chronic nonspecific gingivitis". The
inflammation may be localized to the anterior
region only or may be generalized.
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23.  Etiology:
The causes of chronic gingivitis are
primarily of local nature though there may be
systemic predisposing factors.
 The local irritants include:
 Plaque.
 Calculus.
 Tooth eruption.
 Malocclusion.
 Disuse.
 Mouth breathing.23

24.  The systemic causes (predisposing factors)
include:
 Hormonal disturbances.
 Diabetes mellitus.
 Other factors as blood dyscrasias &
nutritional deficiencies. The systemic
predisposing factors may be of subclinical
nature.
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25.  Clinical Appearance:
The gingival tissue loses its normal
characteristics, instead of the pale, pink
stippled appearance; the gingiva looks red at
the marginal zone with loss of stippling. False
(pseudo) pockets form as a result of gingival
enlargement. The gingiva may bleed on the
slightest touch or eating moderately rough
food as fresh vegetable or fruits.
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26. Treatment:
All of the predisposing factors whether
local or systemic should be considered as
contributors to chronic nonspecific gingivitis
and should be corrected in the treatment of the
condition.
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27. III. Conditioned Gingival Enlargement:
Enlargement of the gingiva is related to
local conditions such as hygiene, food
impaction, mouth occlusal interferences. A
systemic condition is present in many cases.
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28. 1. Puberty Gingival Enlargement:
This is a variety of gingivitis associated
with puberty and characterized by
enlargement of the gingiva. It is usually
somewhat more severe than that
encountered in chronic gingivitis.
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29. Clinical Characteristics:
The gingival enlargement is usually
confined to the anterior segment in the
presence of local irritants. The interdental
papillae are bulbous and prominent far in
excess of the size of gingival enlargement
associated with local factor only. The gingival
margin is red and bleeds on the slightest touch.
Tooth brushing is usually found to have been
avoided by such patients due to excessive
bleeding.
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30. Etiology:
Pubertal gingivitis may be attributed to the
hormonal changes occurring during the
prepubertal and pubertal period which favor an
exaggerated tissue response to local irritants
such as plaque and calculus, in addition to
subclinical nutritional deficiencies due to faulty
dietary habits (smoking, quick meals .... etc.).
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31.  Treatment:
1) Removal of local irritants, improvement of
the oral hygiene, and dietary
recommendation to ensure adequate
nutritional status.
2) At times, the gingival enlargement during
adolescence will regress spontaneously at
above the age of 18, although surgical
intervention may be necessary to restore
gingival margin.
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32. 2. Gingival Fibromatosis (Idiopathic or
Familial):
A rare type of gingival enlargement of
unknown cause although its occurrence may
follow a familial pattern.
 Clinical characteristics:
The gingival enlargement involves the
free and attached gingiva but not the alveolar
mucosa. The painless enlarged tissue may
become as firm and dense as to feel on
palpation like bone. The colour is normal or
slightly paler with coarse stippling.32

33. • Gingival deformity is the main complaint. The
enlargement is symmetrical but may be
unilateral, and may be localized or generalized.
• The gingival tissues apparently look normal at
birth, but begin to enlarge with the eruption of
the primary teeth, in some children by the
eruption of the anterior permanent teeth and in
others by the eruption of posterior teeth and
usually continue to enlarge until the tissue
essentially cover the clinical crowns of the
teeth.
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34. • The fibrous tissue may actually retard the
eruption of teeth into the oral cavity, although
there is normal eruption of the teeth from the
alveolus. The dense fibrous tissue causes
displacement of the teeth. During mastication
the gingiva may become traumatized and
secondary inflammation develops. Local
factors, while present, appear to be secondary
rather than primary etiologic agents.
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35. Treatment:
The treatment is generally unsatisfactory,
gingivectomy of the hyperplastic tissue is done
in several stages. In some persons, slow
regrowth of the fibrous gingival tissue in the
operated areas occur. Recurrence has not been
observed following the removal of the teeth
and the construction of dentures.
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36. 3. Dilantin Gingival Hyperplasia:
Diphenylhydantoin sodium is widely used in
the control of epilepsy. One of the minor side
effects of this drug is a tendency to produce
extensive gingival hyperplasia. The cause of
this reaction is unknown. The gingival tissues
are the only structures affected. Gingival
enlargement occurs in about 50% of all
patients which develops after few weeks from
the therapy. Children and young adults
experience more hyperplasia than adults.
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37. Clinical characteristics:
The clinical appearance varies according to
the age at which the dilantin therapy is
initiated. In children, before eruption of
permanent teeth it may cause delayed eruption
of the permanent dentition. In adolescents, the
gingival changes appear first in the teeth. The
tissue tends to be lobulated and granular in
appearance. If secondary inflammation
occurred, this granular and stippled appearance
is lost. The degree of inflammation is
correlated to the amount of local irritants.
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38. Treatment:
Treatment depends on the degree of severity
of the hyperplasia.
Elimination of the local irritants is essential
in preventing or retarding regrowth of
tissues. In mild cases, interdental
stimulation, effective oral hygiene measures
may result in disappearance of the
enlargement or prevent its further
development. In extensive cases, surgical
removal of the tissues is the only
satisfactory measure.38

39. • Antihistaminic drugs have been used with
limited success, where possible, the
cooperation with the physician should be
thought and an alternative drug is used.
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40. 4. Scorbutic Gingivitis:
Of all vitamins, vitamin C (ascorbic acid)
is the one most likely to affect the
periodontal tissues. The chief function of
ascorbic acid is the development of the
intercellular substance (collagen) of
connective tissue, bone and dentin. Vitamin
C deficiency is associated with hemorrhagic
phenomenon that may result from a defect in
the cementing substance of the capillary
epithelium.
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41. • Experimental deficiency causes a decrease in
the fiber content of periodontal tissues owing
to the inhibition of the normal replacement.
Defects in the integrity of the walls of the
capillaries cause increased capillary fragility
and hemorrhage.
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42. Oral aspects:
Relative deficiency states of vitamin C are
more common than true severe cases (scurvy).
The mild cases may be manifested by impaired
wound healing, follicular hyperkeratosis,
petechiae, possibly chronic gingivitis and a
tendency to hematoma formation.
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43. • In mild cases, the interdental papilla and the
marginal gingiva are swollen and bleed easily
on slightest touch. Unless vitamin C is
instituted in the tissue, secondary infection is a
common complication. Local irritating factors
are necessary to initiate the inflammation.
• In children, true cases of severe (acute)
vitamin C deficiency are rare nowadays.
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44. Therapeutic considerations:
There is no indication for supplemental or
clinical therapeutic administration of
vitamin C unless there are clinical or
laboratory findings suggestive of scurvy.
Correction of the diet is advised and
improvement of oral hygiene is established.
The usual therapeutic dose of vitamin C is
from 100 to 300 mg/ day in divided doses.
Still better, polyvitamins preparation is
prescribed to correct other vitamin
deficiencies.
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45. • Papillon Lefevere Syndrome:
A rare disease inherited as an autosomal
recessive trait. In many cases there is evidence of
parental consanguinity. It is associated with
gingival inflammation and exfoliation of both
primary and permanent dentition. The
hyperkeratosis is limited to the palms of the hands
and soles of the feet.
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46. • The periodontal involvement and alveolar bone
loss start between the second and third year and
progress rapidly thereafter so that by the fourth to
fifth year of age all the primary teeth are lost. The
inflammation subsides after tooth loss. The same
cycle accompany the permanent teeth. The
prognosis is bad and complete dentures are
inserted at an early age.
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47. Thank You
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