gingival diseases in children

Presented by : Najma
M.I.Alamami
Supervised by : Prof. Dr. Nadia
AzizTopics in pediaTric denTisTry 08
607

ouTlines:
 Introduction .
 criteria of healthy gingival tissue
 Classification of gingival diseases.
 Eruption Gingivitis
 Dental Plaque Induced Gingivitis
 Allergy And Gingival Inflammation
 Acute Gingival Disease
1) Herpes Simplex Virus Infection.
2) Recurrent Aphthous Ulcer (Canker Sore).
3) Acute Necrotizing Ulcerative Gingivitis (Vincent Infection)
4) Acute Candidiasis (Thrush, Candidosis, Moniliasis).
5) Acute Bacterial Infections.

ouTlines:
 Chronic Nonspecific Gingivitis.
 Gingival Diseases Modified By Systemic Factors
1) Gingival Diseases Associated With The Endocrine System
2) Gingival Lesions of Genetic Origin.
3) Drugs Induced Gingival Overgrowth.
4) Ascorbic Acid Deficiency Gingivitis (Scorbutic Gingivitis)

Introduction
The gingiva is the part of the
oral mucous membrane that
covers the alveolar processes
and the cervical portions of
the teeth.

Cont…..<<<
The free gingiva is the tissue coronal to the bottom of
the gingival sulcus.
The attached gingiva extends apically from the free
gingival groove to the mucogingival junction.

criteria of healthy gingival
tissue

criteria of healthy gingival tissue
criteria adult child
color light pink more reddish due to increased vascularity
and thinner epithelium.
The surface of the
gingiva (stippling )
stippled less stippled or smoother
the marginal gingiva sharp,
knifelike
edge
During the period of tooth eruption in the
child, the gingivae are thicker and have
rounded margins due to the migration and
cervical constriction of the primary teeth.
depths around tooth Normally
3mm
to be approximately 2 mm, with the facial
and lingual probe sites shallower than the
proximal sites
Periodontal ligament normal
width
wider periodontal ligament than the adult

Note:
 width of the attached gingiva is narrower in the mandible
than in the maxilla, and both widths increase with the
transition from the primary to permanent dentition
The alveolar bone surrounding the
primary dentition demonstrates
fewer trabeculae, less calcification,
and larger marrow spaces

Gingivitis
Definition :
is inflammation of the gingiva that does not result in
clinical attachment loss .

Classification of gingival diseases.
Eruption Gingivitis
Dental Plaque
Induced GingivitisAllergy And Gingival
Inflammation
Acute Gingival Disease
1)Herpes Simplex Virus Infection.
2)Recurrent Aphthous Ulcer
3)ANUG
4)Acute Candidiasis
5)Acute Bacterial Infections
Chronic
Nonspecific
Gingivitis.
Gingival Diseases Modified
By Systemic Factors
1)Gingival Diseases Associated
With The Endocrine System
2) Gingival Lesions of Genetic
Origin.
3)Drugs Induced Gingival
Overgrowth.
4)Ascorbic Acid Deficiency
Gingivitis (Scorbutic Gingivitis)

Microscopically:
1) inflammatory exudate .
2) Edema .
3) some destruction of collagenous.
4) and ulceration and proliferation
of the epithelium facing the tooth
and attaching the gingiva to it.

Etiologic Factors
 Bacterial plaque, which is composed of soft bacterial
deposits that adhere firmly to the teeth, consisting of
dense masses of microorganisms embedded in an
intermicrobial matrix (biofilm).
 In sufficient concentration it can disturb the host-parasite
relationship and cause gingival and periodontal disease.
Calcified(calculus)Uncalcified:

1(ERUPTION GINGIVITIS
 A transitory type of gingivitis is often observed in
young children when the primary teeth are
erupting.
 often localized and associated with difficult
eruption, subsides after the teeth emerge into the
oral cavity.

 The greatest increase in the incidence of gingivitis in
children is often seen in the 6- to 7-year age group
when the permanent teeth begin to erupt.
 This inflammation is most commonly associated with
the eruption of the first and second permanent molars,
and the condition can be painful and can develop into
a pericoronitis or a pericoronal abscess.

Cause:
 This increase in gingivitis apparently occurs because
the gingival margin receives no protection from the
coronal contour of the tooth during the early stage
of active eruption, where Food debris, materia alba,
and bacterial plaque often collect around and
beneath the free tissue, partially cover the crown of
the erupting tooth, and cause the development of
an inflammatory process.

treatment
 Mild eruption gingivitis requires no treatment
other than improved oral hygiene.
 Painful pericoronitis may be helped when the
area is irrigated with a counterirritant, such as
Peroxyl.
 Pericoronitis accompanied by swelling and lymph
node involvement should be treated with
antibiotic therapy.

definition A transitory type of gingivitis is often observed in young children when
the primary teeth are erupting.
group 1) seen in the 6- to 7-year
2) associated with the eruption of the first and second permanent molars
cause during the early stage of active eruption, where Food debris, materia
alba, and bacterial plaque often collect around and beneath the free
tissue
treatment Mild eruption gingivitis requires no treatment other than
improved oral hygiene.
 Painful pericoronitis may be helped when the area is irrigated
with a counterirritant, such as Peroxyl.
 Pericoronitis accompanied by swelling and lymph node involvement
should be treated with antibiotic therapy.

pericoronitis

2(DENTAL PLAQUE INDUCED GINGIVITIS
 The degree of dental cleanliness and the condition of
the gingival tissues in children are related.
 Adequate mouth hygiene and cleanliness of the teeth
are related to frequency of brushing and the
thoroughness with which bacterial plaque is removed
from the teeth.

2(DENTAL PLAQUE INDUCED GINGIVITIS
 Gingivitis is generally less severe in children than in
adults with similar plaque levels.
 Gingivitis associated with poor oral hygiene is
usually classified as:
1)early (slight).
2)Moderate.
3)advanced.
 the importanceof a good standard of oral
cleanliness in reducing gingivitis and, ideally,
preventing the progression of the disease in later
life.

Gingival health was greatly improved
after a thorough plaque removalregimen
was initiated at home.a
Localized gingival infl ammation and
recession associated with minimal plaque
accumulation on mandibular right central
incisor

3(ALLERGY AND GINGIVAL INFLAMMATION
 Matsson and Moller studied the degree of seasonal
variation of gingival infl ammation in children with
allergies to birch pollen.
 Gingival inflammation and the presence or absence
of plaque.
 gingival infl ammatory reaction in the allergic
children during the pollen seasons.
 gingival reaction during short allergic seasons is
difficult to assess.

4(Acute Gingival Disease
A. Herpes Simplex Virus Infection.
B. Recurrent Aphthous Ulcer (Canker Sore).
C. Acute Necrotizing Ulcerative Gingivitis (Vincent
Infection)
D. Acute Candidiasis (Thrush, Candidosis, Moniliasis).
E. Acute Bacterial Infections.

A) HERPES SIMPLEX VIRUS INFECTION
Herpes virus causes one of the most widespread
viral infections.
The primary infection usually occurs in a child
younger than 6 years of age who has had no
contact with
the type 1 herpes simplex virus (HSV-1) and who
therefore has no neutralizing antibodies.
 It is believed that 99% of all primary infections
are of the subclinical type.
The infection may also occur in susceptible
adults who have not had a primary infection

Cont…..<<<
 the primary infection may be manifested by acute
symptoms (acute herpetic gingivostomatitis). which
runs a course of 10 to 14 days.
 The active symptoms of the acute disease can occur in
children with clean mouths and healthy oral tissues.
 May be characterized by only one or two mild sores on
the oral mucous membranes, which may be of little
concern to the child or may go unnoticed by the
parents.

Cont…..<<<
The symptoms of the disease develop suddenly
and include :
 fiery red gingival tissues.
 Malaise.
 irritability.
 headache.
 and pain associated with the intake of food
and liquids of acid content.

characteristic oral finding in the acute primary disease
1) Is the presence of yellow or white liquid-fi lled vesicles.
2) In a few days the vesicles rupture and form painful ulcers 1
to 3 mm in diameter .
3) covered with a whitish gray membrane and have a
circumscribed area of inflammation.
4) The ulcers may be observed on any area of the mucous
membrane, including buccal mucosa,tongue, lips, hard and
soft palate, and the tonsillar areas.
5) Large ulcerated lesions may occasionally be observed on
the palate or gingival tissues or in the region of the
mucobuccal fold.
6) This distribution makes the differential diagnosis more diffi
cult.

Cont……<<<
 Primary herpetic infection has been observed on the
dorsal surface of the thumb of a pediatric patient The
child was a thumb sucker, and the acute primary
infection was present in the mouth.
 The dorsal surface of the thumb, which rested on the
lower incisor teeth, apparently became irritated, and
an inoculation of the virus took place.
 The oral condition and the lesions on the thumb
subsided in 2 weeks.
Primary herpetic infection involving the dorsal
surface of the thumb of a 3-year-old child. An acute
primary infection was present in the mouth.

Several large, painful
ulcers are evident on
the
tongue of a preschool
child with acute herpetic
gingivostomatitis.
Note:
An additional diagnostic criterion is a fourfold rise
of serum antibodies to HSV-1.
The lesion culture also shows positive results for
HSV-1.

Treatment of acute herpetic gingivostomatitis
in children
the treatments described may be useful, they are only palliative..
A. specifi c antiviral medication as well as provision for the relief
of the acute symptoms .
B. The application of a mild topical anesthetic, such as dyclonine
hydrochloride (0.5%) (Dyclone), before mealtime temporarily
relieves the pain .
C. allows the child to take in soft food..
D. Because fruit juices are usually irritating to the ulcerated area,
ingestion of a vitamin supplement during the course of the
disease is indicated.
E. Bed rest .
F. isolation from other children .

vitamins
antiviral topical anesthetic

Examples of drugs used:
 The antiviral medications currently available are acyclovir, famciclovir, and
valacyclovir. These medications inhibit viral replication in cells infected
with the virus. shouldbe administered in five daily doses to equal 1000 mg
per day for 10 days.
 mainstay of definitive therapy is regular doses of specifi c systemic
antiviral medication combined with systemic analgesics (acetaminophen
or ibuprofen) during the course of the disease.
 Another topical anesthetic, lidocaine (Xylocaine Viscous), can be
prescribed for the child who can hold 1 teaspoon of the anesthetic in the
mouth for 2 to 3 minutes and then expectorate the solution
 Schaaf recommends as an alternative to the anesthetic a mixture of equal
parts of diphenhydramine (Benadryl) elixir and Kaopectate. The
diphenhydramine has mild analgesic and antiinfl ammatory
properties,whereas the kaolin-pectin compound coats the lesions.

Ulcerative stage of primary
herpetic gingivostomatitis:(a) palatal
gingiva; (b) lower lip mucosa.

recurrent herpes labialis (RHL(.
 After the initial primary attack during early childhood,
the herpes simplex virus becomes inactive and resides
in sensory nerve ganglia.
 The virus often reappears later as the familiar cold sore
or fever blister, usually on the outside of the lips .
 approximately 5% of recurrences are intraoral.

Recurrent herpes labialis.
A, Early vesicular lesions.
B, Mature vesicular lesion.
C, Appearance of herpes labialis after
rupture of vesicles and crusting of the lesion.
A
B
C

The recurrence of the disease has often been related to:
1) emotional stress .
2) lowered tissue resistance resulting from various types
of trauma.
3) Excessiveexposure to sunlight. Use of sun screen can
prevent sun-induced recurrences.
4) Lesions on the lip may also appear after dental
treatment and may be related to irritation from rubber
dam material or even routine daily procedures.

Herpetic 'cold sore' at the
vermilion border.

recurrent herpes labialis (RHL(.
treatment
 systemic antiviral medications daily dosages are the same as
those for the primary infection, but the course of treatment is
usually 5 days instead of 10.
 Food and Drug Administration (FDA) in children 12 years and
older is valacyclovir 2 g, initially and 2 g 12 hours later.
 topical antiviral agent, penciclovir Cream may be applied to
perioral lesions but should not be applied to intraoral lesions
Every 2 hours while awake for 4 days, and it is approved for use
in children 12 years of age and older.
 Topical 5% acyclovir cream may be prescribed for use five times
daily for 4 days in children 12 years of age and older are
frequently exposed to HSV-1.

B)RECURRENT APHTHOUS ULCER
(CANKER SORE(
Definition :
is a painful ulceration on the unattached mucous
membrane that occurs in school-aged children and
adults.
also referred to as recurrent
aphthous stomatitis (RAS)

(CANKER SORE(
The peak age is between 10 and 19 years of age.
characterized by :
 recurrent ulcerations on the moist mucous
membranes of the mouth, in which both discrete and
confluent lesions form rapidly in certain sites and
feature .
 round to oval crateriform base, raised reddened
margins, and pain.

(CANKER SORE(
Classified to :
Minor
Major
herpetifom
less common and has been referred to as
periadenitis mucosa necrotica recurrens
and Sutton disease.

Etological factors
The cause of RAU is unknown.But It is possible that the
lesions are caused by :
 Local and systemic conditions &gastrointestinal
disorders.
 genetic predisposition.
 immunologic and infectious microbial factors.
 delayed hypersensitivity to the L form of Streptococcus
sanguis,
 autoimmune reaction of the oral epithelium.
 Local factors include trauma, allergy to toothpaste
constituents (sodium lauryl sulfate), and salivary gland
dysfunction.

Etological factors
 Nutritional defi ciencies are found in 20% of persons
with aphthous ulcers.
 The clinically detectable deficiencies include
deficiencies of iron, vitamin B12, and folic acid.
 Stress
 Ship and colleagues also suggested herpes simplex
virus, humanherpesvirus type 6, cytomegalovirus,
Epstein-Barr virus,and varicella-zoster virus as possible
causes of RAS

RAS has been associated with other systemic diseases:
 PFAPA (periodic fever, aphthous stomatitis, pharyngitis,
adenitis), Behçet disease,
 Crohn disease,
 ulcerative colitis,
 celiac disease,
 neutropenia,
 immunodefi ciency syndromes,
 Reiter syndrome,
 systemic lupus erythematosus,
 MAGIC (mouth and genital ulcers with infl amed
cartilage)syndrome.

Treatment of RAU
 Lesions persist for 4 to 12 days and heal
uneventfully, leaving scars only rarely and only in
cases of unusually large lesions .
 Current treatment is focused on:
1) promoting ulcer healing,
2) reducing ulcer duration and patient pain,
3) maintaining the patient’s nutritional intake,
4)and preventing or reducing the frequency of
recurrence of the disease.

A variety of treatments have been recommended for RAU,
but a completely successful therapy has not been found.
 topical gels, creams, and ointments as antiinfl ammatory
agents.
 analgesic medicines and/or systemic immuno-
modulating and immunosuppression agents .ex : topical
corticosteroid (e.g., 0.5% fl uocinonide, 0.025%
triamcinolone, 0.5% clobetasol) is applied to the area
with a mucosal adherent (e.g., isobutyl cyanoacrylate,
Orabase) before meals and before sleeping may also be
helpful or four times daily.

Cont….. <<<
 The topical application of tetracycline to the ulcers is often
helpful in reducing the pain and in shortening the course of
the disease.
 A mouthwash containing suspension of one of the
tetracyclines has been helpful to some, but the mouthwash
should not be swallowed.
 Chlorhexidine mouthwash has also been known to
alleviate the symptoms of RAU.

recurrent aphthous ulcer.
Minor
Major
herpetifom

C) ACUTE NECROTIZING ULCERATIVE
GINGIVITIS (VINCENT INFECTION(
 rare among preschool children .
 occurs occasionally in children 6 to 12 years old,
and is common in young adults.

ANUG can be easily diagnosed because of the involvement
of the interproximal papillae and the presence of a
pseudomembranous necrotic covering of the marginal
tissue

The clinical manifestations of the disease include:
 inflamed, painful, bleeding gingival tissue,
 poor appetite,
 temperature as high as 40°C (104°F),
 general malaise,
 and a fetid odor.

Causitive agent :
Two microorganisms, Borrelia vincentii And fusiform
bacilli, referred to as spirochetal organisms, are
generally believed to be responsible for the disease.

Treatment :
The disease responds dramatically within 24 to 48 hours to :
1) subgingival curettage,
2) débridement,
3) use of mildoxidizing solutions.
4) If the gingival tissues are acutely and extensively infl amed
when the patient is first seen, antibiotic therapy is indicated.
5) Improved oral hygiene,
6) the use of mild oxidizing mouth rinses after each meal, and
twicedaily rinsing with chlorhexidine will aid in overcoming
theinfection.

A) rare example of necrotizing
ulcerative gingivitis in an 8-year-old
boy.
B) Local treatment and improved oral
hygiene produced a dramatic recovery
from the infection.
A
B

A 5-year-old Ethiopian boy
with necrotizing ulcerative gingivitis.

distinguishing ANUG
from acute herpetic gingivostomatitis
criteria acute herpetic
gingivostomatitis
ANUG
shap Round ulcers with
red areolae
on the lips and
cheeks
involvement of the interproximal
papillae and the presence of a pseudo-
membranous necrotic covering of the
marginal tissue
Therapeutic(antibi
otics) prophylaxis
and débridement
not response in the
viral infection.
a favorable response in cases of
ANUG&reduces the acute symptoms in
ANUG.
Age group most frequently
seen in preschool
children
Rarely occurs in the preschool-aged
group
onset onset is rapid develops over a longer period, usually in
a mouth in which irritants and poor oral
hygiene are present

distinguishing ANUG
from acute herpetic gingivostomatitis
acute herpetic
gingivostomatitis
ANUG

D) ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS,
MONILIASIS(
 The lesions of the oral disease appear as raised, furry,
white patches, which can be removed easily to produce
a bleeding underlying surface
 Neonatal candidiasis, contracted during passage through
the vagina and eruptingclinically during the fi rst 2
weeks of life, is a common occurrence. This infection is
also common in immunosuppressed Patients.
 sometimes develop thrush after local antibiotictherapy .

MONILIASIS(

MONILIASIS(
Treatment :
Antifungal antibiotics control thrush.
 For infants and very young children, a suspension of 1 mL
(100,000 U) of nystatin (Mycostatin) may be dropped into
the mouth for local action four times a day. The drug is
nonirritating and nontoxic.
 Clotrimazole suspension (10 mg/mL), 1 to 2 mL applied to
affected areas four times daily, is an effective antifungal
medication.
 Systemic fluconazole suspension (10 mg/mL) is safe to use in
infants at a total dosage of 6 mg/kg or less per day.

Treatment
cont…..<<< :
 For children old enough to manage solid medication
allowed to dissolve in the mouth, clotrimazole troches
or nystatin pastilles are recommended, because the
therapeutic agent remains in the saliva longer than with
the liquid medication.
For children old enough to swallow,
systemic fluconazole (100-mg tablets) in a 14-
day course may be prescribed for patients
whose infection has not responded to topical
antifungal agents.

E) ACUTE BACTERIAL INFECTIONS
 The prevalence of acute bacterial infection in the
oral cavity is unknown.
 acute streptococcal gingivitis with painful, vivid red
gingivae that bled easily was reported .
 The papillae had enlarged, and gingival abscesses
had developed.
 Cultures showed a predominance of hemolytic
streptococci.

E) ACUTE BACTERIAL INFECTIONS
treatment :
 Broad-spectrum antibiotics are recommended if the
infection is believed to be bacterial in origin.
 Improved oral hygiene is important in treating the
infection.
 chlorhexidine mouth rinses are also appropriate.
 The placement of dental restorations to restore
adequate function and contour after the reduction
of acute symptoms is equally important

5(CHRONIC NONSPECIFIC GINGIVITIS
 A type of gingivitis commonly seen during the
preteenage and teenage years .
 May be localized to the anterior region, or it may be
more generalized.
 Although the condition is rarely painful, it may
persist for long periods without much improvement

Characterized by :
 the fiery red gingival lesion is not accompanied by enlarged
interdental labial papillae or closely associated with local
irritants.
 The gingivitis showed little improvement after a prophylactic
treatment.
 The age of the patients involved and the prevalence of the
disease in girls suggested a hormonal imbalance as a possible
factor.
 Histologic examination of tissue sections and the use of
special stains ruled out a bacterial infection.

Ethological factors:
 multitude of local and systemic factors.
 dietary inadequacies
 Inadequate oral hygiene.
 Malocclusion, and crowded teeth, which make oral hygiene
and plaque removal more difficult,
 Carious lesions with irritating sharp margins .
 faulty restorations with overhanging margins.
 mouthbreathing is often responsible for the development
of the chronic hyperplastic form of gingivitis, particularly
in the maxillary arch.

Malocclusionfaulty restorations
overhanging margins
mouthbreathing

Treatment :
An improved dietary intake of vitamins and
the use of multiple-vitamin supplements will
improve the gingival condition in many
children.
Improved oral hygiene.

6(Gingival Diseases Modified By
Systemic Factors
A. Gingival Diseases Associated With The Endocrine
System
B. Gingival Lesions of Genetic Origin.
C. Drugs Induced Gingival Overgrowth.
D. Ascorbic Acid Deficiency Gingivitis (Scorbutic
Gingivitis)

A) GINGIVAL DISEASES ASSOCIATED
WITH THE ENDOCRINE SYSTEM
 Puberty gingivitis is a distinctive type of gingivitis that
occasionally develops in children in the prepubertal and
pubertal period.
 The gingival enlargement was marginal in distribution
and, in the presence of local irritants, was characterized
by prominent bulbous inter proximal papillae far
greater than gingival enlargements
 associated with local factors.
 anterior segment and may be present in only one arch.
 The lingual gingival tissue generally remains
unaffected .

Treatment
 improved oral hygiene,
 removal of all local irritants,
 restoration of carious teeth,
 dietary changes necessary to ensure an adequate
nutritional status.
 oral administration of 500 mg of ascorbic acid.
However, the improvement did not occur until the
vitamin had been taken for approximately 4 weeks.

 Severe cases of hyperplastic gingivitis that do not
respond to local or systemic therapy should be
treated by gingivoplasty.. Recurrence of any
hyperplastic tissue will be minimal if adequate oral
hygiene is maintained.

B) GINGIVAL LESIONS OF GENETIC
ORIGIN
 Hereditary gingival fibromatosis
(HGF) .
 This rare type of gingivitis has
been referred to as elephantiasis
gingivae or hereditary
hyperplasia of the gums
 is characterized :by a slow,
progressive, benign enlargement
of the gingivae.
 has an autosomal dominant
mode of inheritance.

B) GINGIVAL LESIONS OF GENETIC
ORIGIN
 The gingival tissues appear normal at birth but begin
to enlarge with the eruption of the primary Teeth.
 the gingival tissues usually continue to enlarge with
eruption of the permanent teeth until the tissues
essentially cover the clinical crowns of the teeth .
 The dense fibrous tissue often causes displacement of
the teeth and malocclusion.
 The condition is not painful until the tissue enlarges
to the extent that it partially covers the occlusal
surface of the molars and becomes traumatized
during mastication

B) GINGIVAL LESIONS OF GENETIC ORIGIN

histologically
 as a moderate hyperplasia of the epithelium,with
hyperkeratosis and elongation of the rete pegs.
 The increase in tissue mass is primarily the result of
an increase and thickening of the collagenous
bundles inthe connective tissue stroma.
 The tissue shows a high degree of differentiation,
and a few young fi broblasts are present.

histologically

Treatment :
 Surgical removal of the hyperplastic tissue achieves
a more favorable oral and facial appearance.
 Hyperplasia can recur within a few months after the
surgical procedure and can return to the original
condition within a few years.
 importance of excellent plaque control should be
stressed to the patient because this delays the
recurrence of the gingival overgrowth.

C)Drugs -INDUCED GINGIVAL
OVERGROWTH
Many drugs that have been reported to induce
gingival overgrowth in some patients include:
1) Phenytoin (Dilantin, or diphenylhydantoin)
anticonvulsant.
2) cyclosporin.
3) calcium channel blockers
4) valproic acid.
5) and phenobarbital.

PHENYTOIN-INDUCED GINGIVAL OVERGROWTH
 Phenytoin (Dilantin, or diphenylhydantoin), a major
anticonvulsant agent used in the treatment of
epilepsy.
 side effects of varying degrees of gingival hyperplasia
first described by Kimball in 1939.
 phenytoin-induced gingival overgrowth.
an increase in the number of fibroblasts in patients
receiving Dilantin.

PHENYTOIN-INDUCED GINGIVAL
OVERGROWTH

OVERGROWTH
, begins to appear as :
Early as 2 to 3 weeks after initiation of phenytoin therapy
and peaks at 18 to 24 months.
The initial clinical appearance is :
 painless enlargement of the interproximal gingiva.
 The buccal and anterior segments are more often
affected than the lingual and posterior segments.
 The affected areas are isolated at first but can become
more generalized later.

OVERGROWTH
 Unless secondary infection or infl ammation is present, the
gingiva appears pink and firm and does not bleed easily on
probing.
 As the interdental lobulations grow, clefting becomes apparent
at the midline of the tooth.
 With time the lobulations coalesce at the midline, forming
pseudopockets and covering more of the crown of the tooth.
 The epithelial attachment level usually remains constant.
 In some cases, the entire occlusal surface of the teeth becomes
covered.
 These lesions may remain purely fibrotic in nature or may be
combined with a noticeable infl ammatory component

OVERGROWTH
Complication :
1) problems of esthetics.
2) diffi culty in mastication.
3) speech impairment.
4) delayed tooth eruption.
5)tissue trauma, and secondary infl ammation leading
to periodontal disease.

PHENYTOIN-INDUCED GINGIVAL OVERGROWTH
dental treatment based on clinical oral signs and symptoms.
1) mild PIGO (less than one third of the clinical crown is covered)
oral hygiene and more frequent dental care.
a series of four consecutive weekly office visits for prophylaxis and
topical stannous fluoride application is recommended.

Cont……<<<
2) moderate PIGO ( one third to two thirds of the clinical crown
is covered)
 oral home care.
 use of an irrigating device may be needed.
 Use of an antiplaque mouth rinse (0.12% chlorhexidine
gluconate) in the device further helps control bacterial
growth.
 Phenytoin levels should be checked (normal therapeutic
 range is 10 to 15 mg/mL).
 If there has been no change, consultation with the patient’s
physician concerning the possibility of using a different
anticonvulsant drug may be helpful.
 surgical removal of the overgrowth may be recommended

Cont……<<<
3) severe PIGO (i.e., more than two thirds of the tooth is
covered) who do not respond to the previously mentioned
therapeutic regimens.
surgical removal is necessary.
scaling and root planing before surgery and meticulous oral
hygiene after surgery .
no PIGO recurrence for as long as 9 months postoperatively.
If surgery is required a second time and the patient has a
history of rapid recurrence, a pressure appliance should be
considered as an adjunct to home oral care.

pressure appliance
 Immediately after the surgical removal of hyperplastic
tissue, an impression was taken and a positive pressure
splint was constructed.
 Periodontal dressings were removed at the end of 1 week,
and the positivepressure appliance was inserted.
 The natural rubber, mouth-protector type of appliance and
the type with a cast chromium-cobalt framework lined
with soft plastic were equally effective.
 The appliance is generally used only at night but may be
worn night and day if such a schedule is required 8 weeks
of therapy..

Preoperative picture showing
gingival enlargement
Intra-operative view
Positive pressure applianceSix months post-operative view

Drug (phenytoin)-induced gingival enlargement in a
12-year-old boy.

D) ASCORBIC ACID DEFICIENCY GINGIVITIS
(SCORBUTIC GINGIVITIS(
 Scorbutic gingivitis is associated with vitamin C
deficiency and differs from the type of gingivitis
related to poor oral hygiene.
 The involvement is usually limited to the marginal
tissues and papillae.
 The child with scorbutic gingivitis may complain of
severe pain, and spontaneous hemorrhage is
evident.

 Severe clinical scorbutic gingivitis is rare in children.
 it may occur in children allergic to fruit juices.
 Inflammation and enlargement of the marginal gingival
tissue and papillae in the absence of local predisposing
factors are possible evidence of scorbutic gingivitis.
Treatment :
daily administration of 250 to 500 mg of ascorbic acid.
Older children and adults may require 1 g of vitamin C
for 2 weeks to speed recovery.

Mild gingivitis caused by a vitamin C defi ciency. The marginal tissue and papillae
were painfully enlarged. A dietary history revealed that the child’s diet was
grossly defi cient in fruits and vegetables. B, Improvement in diet and greater
emphasis on oral hygiene resulted in great improvement in the oral health.

conclusion
 Gingivitis is a reversible disease. Therapy is aimed primarily
at reduction of etiologic factors to reduce or eliminate
inflammation, thereby allowing gingival tissues to heal.
 Appropriate supportive periodontal maintenance that
includes personal and professional care is important in
preventing re-initiation of inflammation.
 Complete dental care, improved oral hygiene, and
supplementation with vitamin C and other water-soluble
vitamins will greatly improve the gingival condition.
 As with all disorders affecting periodontal tissues,
maintaining excellent oral hygiene is the primary key to
successful therapy.

REFERENCES
 Dentistry For The Child & Adolescent,
MCDONALD, 9TH
EDITION.
 The American Academy Of Pediatric Dentistry
(Aapd) Guidelines 2013.
 Pinkham JR. Patient Guidance. In: Pinkham JR,
Casamassimo PS, Fields HW Jr, Mctigue DJ,
Nowak AJ, Eds. Pediatric Dentistry - Infancy
Through Adolescence. 5th
Ed. St Louis, Mo.
Elsevier-saunders Co;pp.113-139, 2012

gingival diseases in children

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