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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:
Etiologic Factors
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.
1(ERUPTION GINGIVITIS
 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.
1(ERUPTION GINGIVITIS
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.
1(ERUPTION GINGIVITIS
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.
treatment
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.
 Gingival Disease in children by >> najma alamami
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)
B)RECURRENT APHTHOUS ULCER
(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.
B)RECURRENT APHTHOUS ULCER
(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.
 Gingival Disease in children by >> najma alamami
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.
C) ACUTE NECROTIZING ULCERATIVE
GINGIVITIS (VINCENT INFECTION(
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
C) ACUTE NECROTIZING ULCERATIVE
GINGIVITIS (VINCENT INFECTION(
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.
C) ACUTE NECROTIZING ULCERATIVE
GINGIVITIS (VINCENT INFECTION(
Causitive agent :
Two microorganisms, Borrelia vincentii And fusiform
bacilli, referred to as spirochetal organisms, are
generally believed to be responsible for the disease.
C) ACUTE NECROTIZING ULCERATIVE
GINGIVITIS (VINCENT INFECTION(
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 .
D) ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS,
MONILIASIS(
D) ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS,
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
5(CHRONIC NONSPECIFIC GINGIVITIS
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.
5(CHRONIC NONSPECIFIC GINGIVITIS
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.
5(CHRONIC NONSPECIFIC GINGIVITIS
Malocclusionfaulty restorations
overhanging margins
mouthbreathing
5(CHRONIC NONSPECIFIC GINGIVITIS
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.
 Gingival Disease in children by >> najma alamami
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 .
A) GINGIVAL DISEASES ASSOCIATED
WITH THE ENDOCRINE SYSTEM
A) GINGIVAL DISEASES ASSOCIATED
WITH THE ENDOCRINE SYSTEM
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.
A) GINGIVAL DISEASES ASSOCIATED
WITH THE ENDOCRINE SYSTEM
 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.
Chronic marginal gingivitis
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
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.
B) GINGIVAL LESIONS OF GENETIC ORIGIN
histologically
B) GINGIVAL LESIONS OF GENETIC ORIGIN
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
PHENYTOIN-INDUCED GINGIVAL
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.
PHENYTOIN-INDUCED GINGIVAL
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
PHENYTOIN-INDUCED GINGIVAL
OVERGROWTH
PHENYTOIN-INDUCED GINGIVAL
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
moderate PIGO
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.
severe PIGO
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.
D) ASCORBIC ACID DEFICIENCY GINGIVITIS
(SCORBUTIC GINGIVITIS(
D) ASCORBIC ACID DEFICIENCY GINGIVITIS
(SCORBUTIC GINGIVITIS(
 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

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Gingival Disease in children by >> najma alamami

  • 1. Presented by : Najma M.I.Alamami Supervised by : Prof. Dr. Nadia AzizTopics in pediaTric denTisTry 08 607
  • 2. 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.
  • 3. 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)
  • 4. Introduction The gingiva is the part of the oral mucous membrane that covers the alveolar processes and the cervical portions of the teeth.
  • 5. 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.
  • 6. criteria of healthy gingival tissue
  • 7. 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
  • 8. 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
  • 9. Gingivitis Definition : is inflammation of the gingiva that does not result in clinical attachment loss .
  • 10. 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)
  • 11. 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.
  • 12. 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:
  • 14. 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.
  • 15. 1(ERUPTION GINGIVITIS  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.
  • 16. 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.
  • 17. 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.
  • 18. 1(ERUPTION GINGIVITIS 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.
  • 20. 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.
  • 21. 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.
  • 23. 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
  • 24. 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.
  • 26. 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.
  • 27. 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
  • 28. 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.
  • 29. 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.
  • 30. 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.
  • 31. 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.
  • 32. 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.
  • 33. 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 .
  • 35. 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.
  • 36. Ulcerative stage of primary herpetic gingivostomatitis:(a) palatal gingiva; (b) lower lip mucosa.
  • 37. 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.
  • 38. 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
  • 39. 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.
  • 40. Herpetic 'cold sore' at the vermilion border.
  • 41. 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.
  • 42. 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)
  • 43. B)RECURRENT APHTHOUS ULCER (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.
  • 44. B)RECURRENT APHTHOUS ULCER (CANKER SORE( Classified to : Minor Major herpetifom less common and has been referred to as periadenitis mucosa necrotica recurrens and Sutton disease.
  • 45. 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.
  • 46. 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
  • 47. 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.
  • 48. 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.
  • 49. 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.
  • 51. 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.
  • 53. 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.
  • 54. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( 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
  • 55. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( 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.
  • 56. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( Causitive agent : Two microorganisms, Borrelia vincentii And fusiform bacilli, referred to as spirochetal organisms, are generally believed to be responsible for the disease.
  • 57. C) ACUTE NECROTIZING ULCERATIVE GINGIVITIS (VINCENT INFECTION( 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.
  • 58. 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
  • 59. A 5-year-old Ethiopian boy with necrotizing ulcerative gingivitis.
  • 60. 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
  • 61. distinguishing ANUG from acute herpetic gingivostomatitis acute herpetic gingivostomatitis ANUG
  • 62. 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 .
  • 63. D) ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS, MONILIASIS(
  • 64. D) ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS, 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.
  • 65. 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.
  • 66. 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.
  • 67. 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
  • 68. 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
  • 69. 5(CHRONIC NONSPECIFIC GINGIVITIS 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.
  • 71. 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.
  • 72. 5(CHRONIC NONSPECIFIC GINGIVITIS Malocclusionfaulty restorations overhanging margins mouthbreathing
  • 73. 5(CHRONIC NONSPECIFIC GINGIVITIS 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.
  • 75. 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)
  • 76. 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 .
  • 77. A) GINGIVAL DISEASES ASSOCIATED WITH THE ENDOCRINE SYSTEM
  • 78. A) GINGIVAL DISEASES ASSOCIATED WITH THE ENDOCRINE SYSTEM 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.
  • 79. A) GINGIVAL DISEASES ASSOCIATED WITH THE ENDOCRINE SYSTEM  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.
  • 81. 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.
  • 82. 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
  • 83. B) GINGIVAL LESIONS OF GENETIC ORIGIN
  • 84. 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.
  • 85. B) GINGIVAL LESIONS OF GENETIC ORIGIN histologically
  • 86. B) GINGIVAL LESIONS OF GENETIC ORIGIN 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.
  • 87. 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.
  • 88. 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.
  • 90. PHENYTOIN-INDUCED GINGIVAL 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.
  • 91. PHENYTOIN-INDUCED GINGIVAL 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
  • 93. PHENYTOIN-INDUCED GINGIVAL 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.
  • 94. 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.
  • 95. 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
  • 97. 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.
  • 99. 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..
  • 100. Preoperative picture showing gingival enlargement Intra-operative view Positive pressure applianceSix months post-operative view
  • 101. Drug (phenytoin)-induced gingival enlargement in a 12-year-old boy.
  • 102. 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.
  • 103. D) ASCORBIC ACID DEFICIENCY GINGIVITIS (SCORBUTIC GINGIVITIS(
  • 104. D) ASCORBIC ACID DEFICIENCY GINGIVITIS (SCORBUTIC GINGIVITIS(  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.
  • 105. 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.
  • 106. 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.
  • 107. 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

Notas do Editor

  1. Their primary etiology is bacterial plaque, which can initiate destruction of the gingival tissues and periodontal attachment apparatus.1,2
  2. CHLORHEXIDINE AS A THERAPEUTIC PLAQUE CONTROL AGENT Chlorhexidine (CH) is a chlorophenyl biguanide with broad antimicrobial activity. It has been used commonly as an antiseptic skin and wound cleanser for presurgical preparation of the patient and as a handwash and surgical scrub for health care personnel. It has also been added as a preservative to ophthalmic products and has been used internally in very dilute concentrations in the peritoneal cavity and urinary bladder. In dentistry, CH has been studied for control of smooth surface caries, for use as a denture disinfectant, and as a plaque control agent. Its use in controlling dental plaque accumulations has received the most attention in dental research. Mouth rinses containing CH have been popular as therapeutic agents in several countries for some time, and in 1986 CH was approved for use in the United States. Two products under the trade names Peridex (Colgate- Palmolive Co., New York, NY) and PerioGard (Zila Pharmaceuticals, Phoenix, Ariz) have received FDA approval as prescription agents. This mouth rinse contains 0.12% CH gluconate as the active ingredient. Widespread use of CH mouth rinses over many years, especially in Europe, has had an excellent safety record. Few adverse side effects have been reported with CH mouth rinses, but their use has been linked to mouth dryness and burning sensations in some persons due to the alcohol base. An alcohol-free product is available. Generalized staining over long-term use and taste alterations have been reported. Poorly defi ned desquamative lesions have been observed in others after the mouth rinse was used. Allergic reactions to CH are rare. If the rinse is inadvertently swallowed, it has essentially little systemic effect due to poor absorption in the gastrointestinal system. Lِe and Schiِtt reported highly signifi cant inhibition of plaque formation and the prevention of gingivitis with use of an aqueous solution of 0.2% CH digluconate as a mouth rinse twice daily with swishing for 1 minute.31 Yankell and associates have shown that dental stain from CH mouth rinse can be signifi cantly reduced with regular use of a tartar-control dentifrice.32 It is important to recognize that the benefi cial use of CH as a therapeutic mouth rinse should be considered adjunctive to the practice of sound conventional plaque control measures as presented in Chapter 11 and elsewhere in this text. A study by Brecx and colleagues regarding the effi cacy of Listerine, Meridol, and chlorhexidine (CH) mouth rinses found CH to be the most effective to supplement habitual mechanical oral hygiene.33 They also found a combination of habitual self-performed and nonsupervised oral hygiene with Listerine or Meridol is more benefi cial for plaque control than the use of mechanical oral hygiene alone. Its adjunctive use would also seem most appropriate for therapy in cases in which attaining adequate plaque control is more diffi cult, such as during illness or convalescence after serious injuries. The rationale to include use of daily antimicrobial mouth rinse to the child and adolescent’s oral hygiene regimens when inadequate plaque control exists to control and prevent periodontal disease and deliver antimicrobial agents to mucosal sites harboring bacteria throughout the mouth thereby complementing plaque control is widely accepted.34,35
  3. Thirty-four allergic children were examined during two successive spring seasons and the one intervening fall. Age- and sex-matched controls were also examined in the fall. Gingival infl ammation and the presence or absence of plaque were recorded, and a bleeding/plaque ratio was calculated for each subject. The results indicated an enhanced gingival infl ammatory reaction in the allergic children during the pollen seasons. Although the authors acknowledge that the signifi cance of gingival reaction during short allergic seasons is diffi cult to assess, they speculate that patients with complex allergies who have symptoms for longer periods may be at higher risk for more signifi cant adverse periodontal changes.
  4. children 12 years of age and older. Other remedies for herpes simplex infection also include the amino acid lysine. The oral therapy is based on lysine’s antagonistic effect on another amino acid, arginine. Griffi th and associates conducted an initial study in which 250 patients were given daily lysine doses of 1000 mg and were told to avoid eating arginine-rich foods, such as chocolate and nuts.16 The lysine therapy was continued until the patients had been lesion free for 6 months. L-Lysine monohydrochloride is available commercially in capsule form or tablets containing 100 or 312 mg of L-Lysine (General Nutrition Corp., Pittsburgh, Pa.). The patients reported that pain disappeared overnight in virtually every instance. New vesicles failed to appear, and a majority considered the resolution of the lesions to be more rapid than in the past. There was also a reduction in frequency of occurrences. Griffi th and colleagues concluded that improper food selection may make adequate lysine intake precarious for some persons.16 Ingestion of cereals, seeds, nuts, and chocolate would produce a high arginine/lysine ratio and favor the development of herpetic lesions. Similar results are obtained when arginine is added to the medium in the laboratory to induce herpes proliferation. The avoidance of these foods, coupled with the selection of foods with adequate lysine, such as dairy products and yeast, should discourage herpes infection
  5. It has been reported to be the most common mucosal disorder in people of all ages and races in the world. It has been reported to be the most common mucosal disorder in people of all ages and races in the world.
  6. antiinfl ammatory and antiallergic medication in the form of a topical paste. The paste is applied to the ulcer four times daily, after meals and at bedtime, until the ulcer heals. Zilactin (Zila Pharmaceuticals, Phoenix, Ariz), a topical paste with hydroxypropyl cellulose fi lm, has also been used to adhere to the mucosa and cover the ulcer while providing pain relief for an extended period of time. Occlusive topical 2-otylcyanoacrylate adheres for 6 hours. Aloe vera freeze-dried gel extract adheres and forms an occlusive protective patch. In severe cases, oral prednisone has been prescribed.
  7. A therapeutic trial of antibiotics reduces the acute symptoms in ANUG but not in the viral infection. Acute herpetic gingivostomatitis is most frequently seen in preschool children, and its onset is rapid. As stated earlier, ANUG rarely occurs in the preschool-aged group and develops over a longer period, usually in a mouth in which irritants and poor oral hygiene are present. On the other hand, acute oral infections initially diagnosed as ANUG have frequently been found later to be an oral manifestation of one of the xanthomatoses. The early stages of conditions such as Hand-Schüller-Christian disease and Letterer- Siwe disease are associated with many of the symptoms of ANUG.
  8. Although the tissue usually appears pale and fi rm, the surgical procedure is accompanied by excessive hemorrhage. Therefore quadrant surgery is usually recommended. Brown and colleagues have reported a case in which apically positioned fl ap surgery and CO2 laser evaporation were used to reduce the gingival tissue.41
  9. Some authors report a positive relationship between the level of phenytoin in serum and saliva and the severity of PIGO in some cases.44-46 Other investigators have reported that no such correlation exists.47,48 It is generally agreed that a relationship exists between dosage and PIGO when the level of phenytoin per unit body weight or actual serum level is considered. Sasaki and Maita reported a signifi cant correlation between the degree of gingival overgrowth and a high level of basic fi broblast growth factor in serum.49 No such correlations were observed for patient age, daily or total phenytoin dose, duration of therapy, or serum phenytoin level.
  10. No cure exists and treatment is often symptomatic in nature. Antihistamines, topical corticosteroids, ascorbic acid (vitamin C) supplements, topical antibiotics, and alkaline mouthwashes have been used with limited success and are considered to be ineffective. Steinberg and Steinberg describe current recommended
  11. less severe type of gingivitis resulting from vitamin C deficiency is probably much more common than most dentists realize.