Gingival and Periodontal

Diseases in Children

DIFFERENCES BETWEEN THE CHILD

AND ADULT PERIODONTIUM

Sulcus depth: Greatermean depth is 2.1+/ 0.2 mm

Free gingiva: Thicker and rounder (cervical bulge and underlying

constriction)

Marginal gingiva: Flaccid and retractable (immature connective tissue

and gingival fiber system and also due to increased vascularization )

Attached gingiva: Greater width

DIFFERENCES BETWEEN THE

CHILD AND ADULT
PERIODONTIUM
Interdental cleft: found in inter-radicular zone and retrocuspid papilla, 1
mm below the free gingival groove lingual to mandibular canine

Periodontal space: wider with few fibers

Alveolar bone:
Less calcifed
More vascular
Few but thicker trabeculae
Larger marrow space
Prominent lamina dura
Flattened interdental crests

Gingivitis: common than periodontitis; more transient and acute

compared to progressive and chronic in adults.

DIFFERENCES BETWEEN THE

CHILD AND ADULT
PERIODONTIUM
Gingivitis rarely progressed to periodontitis in prepubertal children

more anabolic activity due to increase metabolism,

absence of bacteria responsible for periodontal disease such as Spirochetes and

B. melaninogenicus,

altered composition of plaque,

decreased leukocytic migratory rate due to low levels of immunoglobulin

specific for plaque bacteria

decreased vascular inammatory response

But periodontal disease seen in adults may have its origin in childhood
prevention,
early
diagnosis
and
aggressive
treatment
of
gingival and periodontal disease in children.

PHYSIOLOGIC GINGIVAL CHANGES

ASSOCIATED WITH TOOTH ERUPTION

Gingivitis
It is the inammatory involvement of gingival tissue.
Microscopically it is characterized by presence of inammatory
exudate and edema and destruction of collagenous gingival
fibers. Ulcerations of the epithelium are also seen.

Stages of Gingivitis

Stage I: Initial Lesion

A. Time period2 to 4 days
B. Vascular dilatation and vasculitis is seen
C. Junctional and sulcular epithelium are seen intrated by polymorphonuclear
cells
D. Associated with mild change in color.

Stage II: Early Lesion

A. Time period4 to 7 days
B. Increased vascular proliferation
C. Junctional and sulcular epithelium is seen infiltrated by polymorphonuclear
cells, rete pegs formation, atrophic areas
D. Lymphocytes are predominant
E. Loss of collagen
F. Clinical findings include erythema, bleeding on probing.

Stages of Gingivitis

Stage III: Established Lesion

A. Time period14 to 21 days
B. Increased vascular proliferation and blood stasis
C. Changes seen in the junctional and sulcular epithelium are more
severe than stage II
D. Plasma cells are predominant
E. Severe loss of collagen.
F. Clinical fndings include changes in color, size and texture, etc.

Stage IV: Advanced Lesion

A. The lesion extends into alveolar bone
B. Characterized by periodontal breakdown.

Clinical Features of Gingivitis

Gingival bleeding: Two earliest symptoms

Increased gingival uid production rate
Bleeding from gingival sulcus on probing

Change in the color of gingiva:

Normal: coral pink. Inamed tissue: red or bluish red.

Changes in consistency of gingiva:

In chronic inammation, both destructive (edematous) and reparative (fibrotic)
changes co-exist.

Changes in surface texture of the gingiva:

Loss of surface stippling is an early sign of gingivitis.
Chronic inammationthe surface is either smooth and shiny (exudate) or firm
and nodular (fibrotic).

ETIOLOGY OF GINGIVAL DISEASES

I. Local irritating factors

A. Bacterial plaque
B. Predisposing factors like: material alba, food debris, malalignment of teeth,
dental calculus, etc.

II. Local functioning factors

A. Malocclusion
B. Habits: mouth breathing, tongue thrusting
C. Eruption of teeth

III. Systemic factors

A. Puberty
B. Vitamin or protein defciency
C. Drugs and chemicals
D. Pregnancy
E. Hereditary
F. Metabolic disorders
G. Hematological disorder
H. Viral, bacterial and fungal infections.

Classifcation of Gingival Diseases

A. Dental plaque-induced gingival diseases
1. Gingivitis associated with dental plaque only
a. Without other local contributing factors
b. With local contributing factors
2. Gingival diseases modifed by systemic factors
a. Associated with the endocrine system
Puberty-associated gingivitis
Menstrual cycle-associated gingivitis
Pregnancy-associated
+ Gingivitis
+ Pyogenic granuloma
Diabetes mellitus-associated gingivitis
b. Associated with blood dyscrasias
Leukemia-associated gingivitis
Other
3. Gingival diseases modifed by medications
a. Drug-inuenced gingival diseases
Drug-inuenced gingival enlargements

Classifcation of Gingival Diseases

B. Non-plaque-induced gingival lesions
1. Gingival diseases of specifc bacterial origin
a. Neisseria gonorrhoeae-associated lesions
b. Treponema pallidum-associated lesions
c. Streptococcal species-associated lesions
d. Other
2. Gingival diseases of viral origin
a. Herpesvirus infections
Primary herpetic gingivostomatitis
Recurrent oral herpes
Varicella-zoster infections
b. Other
3. Gingival diseases of fungal origin
a. Candida-species infections
Generalized gingival candidiasis
b. Linear gingival erythema
c. Histoplasmosis
d. Other
4. Gingival lesions of genetic origin
a. Hereditary gingival fbromatosis
b. Other
5. Gingival manifestations of systemic conditions
a. Mucocutaneous disorders
Lichen planus
Pemphigoid
Pemphigus vulgaris

Classifcation of Periodontal
Disease

Chronic Periodontitis
A. Localized
B. Generalized
Aggressive Periodontitis
A. Localized
B. Generalized
Periodontitis as a Manifestation of
Systemic Diseases
A. Associated with hematological disorders
1. Acquired neutropenia
2. Leukemias
3. Other
B. Associated with genetic disorders
1. Familial and cyclic neutropenia
2. Down syndrome
3. Leukocyte adhesion defciency syndromes
4. Papillon-Lefvre syndrome
5. Chediak-Higashi syndrome
6. Histiocytosis syndromes
7. Glycogen storage disease
8. Infantile genetic agranulocytosis
9. Cohen syndrome
10. Ehlers-Danlos syndrome (Types IV and VIII)
11. Hypophosphatasia
12. Other
C. Not otherwise specifed (NOS)
Necrotizing Periodontal Diseases
A. Necrotizing ulcerative gingivitis (NUG)
B. Necrotizing ulcerative periodontitis (NUP)
Abscesses of the Periodontium
A. Gingival abscess
B. Periodontal abscess
C. Pericoronal abscess
Periodontitis Associated with Endodontic Lesions
Combined periodontic-endodontic lesions
Developmental or Acquired
Deformities and Conditions
A. Localized tooth-related factors that modify or predispose to plaque-induced gingival diseases/
periodontitis
1. Tooth anatomic factors
2. Dental restorations/appliances
3. Root fractures
4. Cervical root resorption and cemental tears
B. Mucogingival deformities and conditions around teeth
1. Gingival/soft tissue recession
a. Facial or lingual surfaces
b. Interproximal (papillary)
2. Lack of keratinized gingiva
3. Decreased vestibular depth
4. Aberrant frenum/muscle position
5. Gingival excess
a. Pseudopocket
b. Inconsistent gingival margin
c. Excessive gingival display
d. Gingival enlargement
6. Abnormal color
C. Mucogingival deformities and conditions on edentulous ridges
1. Vertical and/or horizontal ridge defciency
2. Lack of gingiva/keratinized tissue
3. Gingival/soft tissue enlargement
4. Aberrant frenum/muscle position
5. Decreased vestibular depth
6. Abnormal color
D. Occlusal trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma

Gingival and periodontal diseases in

children

Gingival Disease
1. Simple gingivitis
a. Eruption gingivitis
b. Gingivitis associated with poor oral hygiene
2. Acute gingival inammation
Herpes simplex virus infection
Recurrent aphthous ulcer
Acute necrotizing ulcerative gingivitis
Acute candidiasis
Acute bacterial infections
3. Chronic non-specifc gingivitis
4. Conditioned gingival enlargement
a. Puberty gingivitis
b. Fibromatosis
c. Phenytoin induced gingival overgrowth
5. Scorbutic gingivitis

Eruption Gingivitis

Seen during the eruption of teeth and subsides soon after

Greatest incidence is 6 to 7 years when permanent teeth begin to erupt

Due to lack of protection to the gingiva from the coronal contour of the tooth

May be painful and develop into pericoronitis or pericoronal abscess

Management:
Mild eruption gingivitis: no treatment + improved oral hygiene.
Painful pericoronitis: irrigating with a counterirritant, such as Peroxyl
Pericoronitis accompanied by swelling and lymph node involvement: antibiotic
therapy.

Gingivitis Associated with Poor

Oral Hygiene

Oral hygiene and gingivitis are directly related

Adequate oral hygiene practice leading to thorough plaque removal and eating raw
fber vegetables and fruits have benefcial effect on reducing gingivitis

It can be grouped as early, moderate and advanced gingivitis

Early gingivitis is quickly reversible and treated with good tooth brushing and
ossing

Moderate and severe gingivitis requires more elaborate measures

Gingivitis Associated with HSV I

Herpes virus
causes one of the most widespread viral infections.
Infection

The primary infection usually occurs in a child younger than 6 years of age
who has had no contact with HSV-1 and who therefore has no neutralizing
antibodies

It rarely occurs before the age of six months, apparently because of the
presence of circulating antibodies in the infant, derived from the mother

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 Herpetic stomatitis is a common oral disease which
develops in both children and young adults

Gingivitis Associated with HSV I

Clinical Feature:
Infection

In some preschool children: only one or two mild sores on the oral mucous membranes
little concern to the child or unnoticed by the parents

In other children: acute symptoms (acute herpetic gingivostomatitis)

The active symptoms of the acute disease can occur in children with clean mouths and
healthy oral tissues these children seem to be as susceptible as those with poor oral
hygiene.
Develop suddenly and include: fever, irritability, headache, pain upon swallowing (pain
associated with the intake of food and liquids of acid content) and regional
lymphadenopathy
Within a few days the mouth becomes painful and the gingiva intensely inamed ; The
lips, tongue, buccal mucosa, palate, pharynx and tonsils may also be involved
Characteristic oral finding: Shortly, yellowish, uid filled vesicle rupture and form
shallow, ragged, extremely painful ulcers (1 3mm) covered by a gray membrane and
surrounded by an erythematous halo; Large ulcerated lesions may occasionally be
observed on the palate or gingival tissues or in the region of the mucobuccal fold
the differential diagnosis more difficult.
Laboratory:

Treatment of Gingivitis
Associated with HSV I Infection
Treatment of acute herpetic gingivostomatitis in
children, which runs a course of 10 to 14 days,
should include specific antiviral medication as
well as provision for the relief of the acute
symptoms so that fluid and nutritional intake
can be maintained.

Treatment of Gingivitis Associated

with HSV I Infection
Palliative Treatment

Definitive Therapy

- Mild topical anesthetic, such as dyclonine

hydrochloride (0.5%) (Dyclone) before
mealtime temporarily relieves the pain
and allows the child to take in soft food
- Lidocaine (Xylocaine Viscous) for the child
who can hold 1 teaspoon of the anesthetic
in the mouth for 2 to 3 minutes and then
expectorate the solution
- A mixture of equal parts of
diphenhydramine (Benadryl) elixir (mild
analgesic and antiinammatory
properties) and Kaopectate (coats the
lesions)
- Vitamin supplement during the course of
the disease

Regular doses of specific systemic

antiviral medication combined with
systemic analgesics (acetaminophen or
ibuprofen)
- Antiviral medications: acyclovir,
famciclovir, and valacyclovir inhibit viral
replication in cells infected with the virus
- Acyclovir (Zovirax) should be
administered in five daily doses to equal
1000 mg per day for 10 days.
- Bed rest and isolation from other children
in the
family

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

Predispoing factors:
Emotional stress
Lowered tissue resistance resulting from various types of trauma.
Excessive exposure to sunlight.
After dental treatment
Rubber dam material
Even routine daily procedures

The most effective treatment for these recurrences is the use of the specific systemic
antiviral medications immediately after the prodromal symptom of recurrence

Treatment of Recurrent herpes

labialis
Acyclovir: The daily dosages are the same as those for the primary infection, but
the course of treatment is usually 5 days instead of 10

Oneday therapy for recurrent herpes labialis (12 years of age and older) is a
total of 4g valacyclovir given in a divided dose; 2g initially with the prodrome,
followed 12 hours later with another 2g

Famciclovir 1500 g one dose with prodrome (earliest sign of the lesions) for adults

Topical antiviral agent for 12 years of age and older:

Penciclovir cream (Denavir): every 2 hours while awake for 4 days applied to
perioral lesions but not intraoral lesions. The penciclovir cream and systemic
antivirals should not be prescribed for concurrent use.

Topical 5% acyclovir cream may be prescribed for use five times daily for 4
days

The lysine therapy: daily lysine doses of 1000 mg (L-Lysine monohydrochloride is

available commercially in capsule form or tablets containing 100 or 312 mg of LLysine)

Avoid arginine food: cereals, seeds, nuts, and chocolate

Selection Lysine rich food: dairy products and yeast

Gingivitis Associated with Aphthous

Stomatitis
Recurrent aphthous ulcer (RAU) Recurrent aphthous stomatitis (RAS)is a painful
ulceration on the unattached mucous membrane
Occur in school-aged children and adults (10 19)
The most common mucosal disorder in people of all ages and races in the world
Characterized by recurrent ulcerations on the moist mucous membranes of the mouth, in
which both discrete and conuent lesions form rapidly in certain sites and feature a round
to oval crateriform base, raised reddened margins, and pain.
Appear as attacks of minor or single, major or multiple, or herpetiform lesions.
Lesions persist for 4 to 12 days and heal uneventfully, leaving scars only rarely and only in
cases of unusually large lesions.
RAS has beenassociated with other systemic diseases: PFAPA (periodic fever, aphthous
stomatitis, pharyngitis, adenitis), Behet disease, Crohn disease, ulcerative colitis, celiac
disease, neutropenia, immunodeficiency syndromes, Reiter syndrome, systemic lupus
erythematosus, and MAGIC (mouth and genital ulcers with inamed cartilage) syndrome.

Cause of RAU

Unknown

Potential causes: Local and systemic conditions along with a genetic predisposition, as well as immunologic
and infectious microbial factors

May be caused by a delayed hypersensitivity to the L form of Streptococcus sanguis or by an autoimmune

reaction of the oral epithelium

RHL and RAU may be produced by the same mechanism, despite the known infectious agent of RHL and the
absence of any known virus for RAU

Local factors include trauma, allergy to toothpaste constituents (sodium lauryl sulfate), and salivary gland
dysfunction

Minor trauma is a common precipitating factor accounting for as many as 75% of the episodes: Injuries
caused by cheek biting and minor facial irritations are probably the most common precipitating factors

Nutritional deficiencies are found in 20% of persons with aphthous ulcers (iron, vitamin B12, and folic acid)

A history of unusually high incidence of gastrointestinal disorders

Stress may prove to be an important precipitating factor, particularly in stress-prone groups, such as
students in professional schools and military personnel

Nonspecific factors (trauma, food allergy) or specific factors (bacterial or viral infection) a temporary
imbalance
in various cell subpopulations upset immune regulation local destruction of the oral epithelium
ulceration

Ship and colleagues also suggested HSV, HHV 6, CMV, EBV, and VZV virus as possible causes of RAS.

Treatment of RAU
Current treatment is focused on:

Promoting ulcer healing,

Reducing ulcer duration and patient pain,

Maintaining the patients nutritional intake,

Preventing or reducing the frequency of recurrence of the disease.

Topical antiinammatory and

analgesic medicines
and/or systemic
immunomodulating and
immunosuppression agents

Treatment of RAU

The primary line of treatment: topical gels, creams, and ointments as antiinammatory agents: a topical
corticosteroid (e.g., 0.5% uocinonide, 0.025% triamcinolone, 0.5% clobetasol) + a mucosal adherent
(e.g., isobutyl cyanoacrylate, Orabase). For example, triamcinolone acetonide (Kenalog in Orabase)
before meals and before sleeping

An antiinammatory and antiallergic medication in the form of a topical paste is effective in reducing pain
and accelerating healing of RAU ulcers. The active ingredient in the paste is 5% amlexanox (Aphthasol).
The paste is applied to the ulcer four times daily, after meals and at bedtime, until the ulcer heals.

Zilactin, a topical paste with hydroxypropyl cellulose film, has also been used to adhere to the mucosa
and cover the ulcer while providing pain relief for an extended period of time.

In severe cases, oral prednisone has been prescribed.

Topical rinses have also been helpful for relief of RAU:

Sucralfate (coating the area);

Topical application of tetracycline (reducing the pain and in shortening the course),

Mouthwash containing suspension of one of the tetracyclines has been helpful to some, but the mouthwash should not
be swallowed;

Chlorhexidine mouthwash (alleviate symptoms);

Swished dexamethasone elixir is useful to treat ulcerations in areas of the mouth that are difficult to access;

Vigorous twice-daily rinsing antimicrobial mouthwash (Listerine) significantly reduces the duration and severity

Varicella-zoster virus may be of etiologic importance in RAU six of eight patients with chronic severe
RAU who were treated with acyclovir responded favorably within 2 days ???

Acute Necrotizing Ulcerative

Gingivitis (ANUG)

Caused by Borrelia vincentii and spirochetes

Severe ulcerating gingivitis involving the interproximal papillae, covered

by a psuedomembrane

Clinical Features: inamed, painful, bleeding gingival tissue, poor

appetite,
temperature as high as 40C (104F), general malaise, fetid odor

Recovery promptly occurs within 36 hours after penicillin therapy and

application of hydrogen peroxide:

The disease responds dramatically within 24 to 48 hours to subgingival

curettage, dbridement, and the use of mild oxidizing solutions.

If the gingival tissues are acutely and extensively inamed when the patient is
first seen, antibiotic therapy is indicated.

Improved oral hygiene, the use of mild oxidizing mouth rinses after each meal,
and twicedaily rinsing with chlorhexidine will aid in overcoming the infection.

ANUG and Acute Herpetic

Gingivostomatitis

Round ulcers with red areolae on the lips and cheeks AHG

Therapeutic prophylaxis and dbridement bring about a favorable response

ANUG

Therapeutic antibiotics reduces the acute symptoms AHG

Most frequently seen in preschool children, and its onset is rapid AHG

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 ANUG

Found later to be an oral manifestation of one of the xanthomatoses; the early

stages of conditions such as Hand-Schller-Christian disease and LettererSiwe
disease ANUG

Associated with Acute Bacterial

Infection

Caused by Streptococci group of bacteria

The gingiva is painful that bleeds easily

Papilla is enlarged with associated gingival abscess

The diagnosis is difficult to make, however, without extensive laboratory

tests.

Treatment includes broad spectrum antibiotics, improvement of oral

hygiene and chlorhexidine mouth wash.

ACUTE CANDIDIASIS (THRUSH, CANDIDOSIS,

MONILIASIS)
Candida (Monilia) albicans is a common inhabitant of the oral
cavity but may multiply rapidly and cause a pathogenic state
when host resistance is lowered.
Young children sometimes develop thrush after local antibiotic
therapy.
The lesions of the oral disease appear as raised, furry, white
patches, removed easily to produce a bleeding underlying
surface.
Neonatal candidiasis, contracted during passage through the
vagina and erupting clinically during the first 2 weeks of life, is a
common occurrence. This infection is also common in
immunosuppressed patients

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

Clotrimazole suspension (10 mg/mL), 1 to 2 mL applied to affected areas

four times daily

Systemic uconazole suspension (10 mg/mL) is safe to use in infants at

a total dosage of 6 mg/kg or less per day

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 uconazole (100-mg

tablets) in a 14-day course may be prescribed for patients whose
infection has not responded to topical antifungal agents.

Associated with Chronic Nonspecifc

Gingivitis

No specific etiology

Hormonal imbalance

Subclinical vitamin deficiency

Malocclusion

Carious lesions with irritating sharp margins, as well as faulty restorations with
overhanging margins

Mouth breathing

The chronic gingivitis group had a larger percentage of AB blood types

It may be localized to the anterior region or may be more generalized

It is rarely painful, but persists for a longer period of time

Since the cause is nonspecific the treatment is limited to maintaining the oral
hygiene and regular professional prophylaxis.

Puberty Gingivitis

Occurs in the prepubertal and pubertal period

Gingival inammation is confned to the anterior segment and

may be limited to single arch only

Gingiva on the lingual aspect is relatively uninvolved

Concerned with maintenance of adequate oral hygiene,

removal of local irritants, and restoration of caries.

Cohen: oral administration of 500 mg of ascorbic acid

(improve after 4w)

Severe cases of hyperplastic gingivitis, not respond to local

or systemic therapy: gingivoplasty (the thickened fibrotic
marginal and interproximal tissue).

Recurrence: maintain adequate oral hygiene.

Hereditary Fibromatosis Gingival

Enlargement
Hereditary gingival fibromatosis (HGF) is characterized by a slow,
progressive, benign enlargement of the gingivae.

Autosomal dominant mode of inheritance

The surface is normal appearing

Appears as soon as the deciduous teeth erupt into the oral cavity
and cover the teeth completely

They are fibrous tending to displace the teeth (malocclusion) and

are nonpainful

They regress only if the teeth are extracted

Surgical excision is the treatment of choice but they recur in a few

months and to the original condition within a period of few years.

Although the tissue usually appears pale and firm, the surgical
procedure is accompanied by excessive hemorrhage quadrant
surgery; apically positioned ap surgery and CO2 laser evaporation

Excellent plaque control delays the recurrence of the gingival

overgrowth.

Drug-induced Hyperplasia
PHENYTOIN-INDUCED GINGIVAL OVERGROWTH

Phenytoin (2 millions taken, 0-95% incidence; average: 40 50%),

an anticonvulsant drug is the commonly seen cause of hyperplasia
of the gingiva. Other drugs that induce hyperplasia are
cyclosporine and Nifedipine.

No such correlations were observed for patient age, daily or total

phenytoin dose, duration of therapy, or serum phenytoin level.

Patients without teeth almost never develop PIGO The

relationship between plaque, local irritants, and PIGO

Appears as early as 2 to 3 weeks after initiation of the phenytoin

therapy and peaks at 18 to 24 months.

Painless enlargement of the gingiva at the interproximal aspect.

Buccal and anterior segment > lingual and posterior segment.

Gingiva appears pink and firm unless infected.

Normally do not bleed readily

Formation of pseudopockets

Problems of esthetics, difficulty in mastication, speech impairment,

delayed tooth eruption, tissue trauma, and secondary
inammation leading to periodontal disease

Treatment of
PHENYTOIN-INDUCED GINGIVAL
OVERGROWTH
Mild PIGO (i.e., less than one third of the clinical crown is covered): daily meticulous
oral hygiene and more frequent dental care

Moderate PIGO (i.e., one third to two thirds of the clinical crown is covered):
meticulous oral home care + the judicious use of an irrigating device with an
antiplaque mouth rinse (0.12% chlorhexidine gluconate)
Initially, a series of four consecutive weekly office visits for prophylaxis and
topical stannous uoride application is recommended.
The fifth week is used to evaluate the gingivae and note any change in size.
Phenytoin levels should be checked (normal therapeutic range is 10 to 15 mg/mL)
consultation with the patients physician concerning the possibility of using a
different anticonvulsant drug surgical removal of the overgrowth may be
recommended.

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. As
in any periodontal surgery, scaling and root planing before surgery and meticulous
oral hygiene after surgery are essential to minimize the overgrowth, which can occur
as early as 3 to 4 weeks after surgery.

Scorbutic Gingivitis

Associated with vitamin C deficiency

Involvement is limited to marginal tissue and papillae

Associated with severe pain, spontaneous hemorrhage

Inammation and enlargement of the marginal gingival tissue and

papillae in the
absence of local predisposing factors are possible evidence of scorbutic
gingivitis

Treatment: Complete dental care, improved oral hygiene, and

supplementation with vitamin C and other water-soluble vitamins

PERIODONTAL DISEASES IN
CHILDREN
Periodontitis,
an inammatory disease of the gingiva and
deeper tissues of the periodontium, is characterized by
pocket formation and destruction of the supporting alveolar
bone.

Bone loss in children can be detected in bite-wing

radiographs by comparing the height of the alveolar bone to
the cementoenamel junction:
Distances between 2 and 3 mm can be defined as
questionable bone loss
Distances greater than 3 mm indicate definite bone loss.
In preschool children with periodontitis, recession, gingival
erythema, and edema are not usually found unless the child
is neutropenic Periodontal probing for attachment loss and
bite-wing radiography are often used to clinically confirm the

PREPUBERTY PERIODONTITIS (AGGRESSIVE

PERIODONTITIS)

Aggressive periodontitis of the primary dentition can occur in a localized form

but usually is seen in the generalized form.

Localized aggressive periodontitis (LAP) is localized attachment loss and

alveolar bone loss only in the primary dentition in an otherwise healthy child.

The exact time of onset is unknown, but it appears to arise around or before 4
years of age, when the bone loss is usually seen on radiographs around the
primary molars and/or incisors.

Abnormal probing depths, minor gingival inammation, rapid bone loss, and
minimal to varying amounts of plaque.

Abnormalities in host defenses (e.g., leukocyte chemotaxis), extensive

proximal caries facilitating plaque retention and bone loss, and a family
history of periodontitis.

As the disease progresses, the childs periodontium shows signs of gingival

inammation with gingival clefts and localized ulceration of the gingival
margin.

PREPUBERTY PERIODONTITIS (AGGRESSIVE

PERIODONTITIS)

The onset of GAP is during or soon after the eruption of the primary teeth.

Severe gingival inammation and generalized attachment loss, tooth mobility, and rapid
alveolar bone loss with premature exfoliation of the teeth.

The gingival tissue may initially demonstrate only minor inammation with a minimum
of plaque material. Chronic cases display the presence of clefting and pronounced recession
with associated acute inammation.

Testing may reveal a high prevalence of leukocyte adherence abnormalities and an impaired
host response against bacterial infections.

Alveolar bone destruction proceeds rapidly, and the primary teeth may be lost by 3 years of
age.

Microorganisms predominating in the gingival pockets include Aggregatibacter

actinomycetemcomitans (Aa), Porphyromonas (Bacteroides) gingivalis,
Bacteroides melaninogenicus, Prevotella intermedia, Capnocytophaga sputigena, and
Fusobacterium nucleatum.

The major periodontal pathogens are transmitted among family members. Often the past
medical history of the child reveals a history of recurrent infections. (e.g., otitis media, skin
infections, upper respiratory tract infections) Consultation with a pediatrician is needed to
rule out systemic diseases.

Treatment of
PREPUBERTY PERIODONTITIS
Treatment of LAP or GAP depends on early diagnosis, dental
curettage, root planing, prophylaxis, oral hygiene instruction,
restoration of decayed teeth, removal of the primary teeth that
have lost bony support, and more frequent recalls.
Use of antimicrobial rinses (chlorhexidine) and therapy with
broad-spectrum antibiotics are effective in eliminating the
periodontal pathogens. Amoxicillin has been used in children
(250-mg liquid three times a day for 10 days).
Treatment of GAP is less successful overall and sometimes
requires extraction of all primary teeth. Delaney reported that
children affected with LAP or GAP may experience severe
periodontitis of the permanent teeth.

LOCALIZED AGGRESSIVE
PERIODONTITIS
Seen in otherwise healthy children

Characterized by rapid and severe loss of alveolar bone around more than one permanent
tooth involving the frst molars and incisors.

Appears self-limiting

No tissue inammation is seen and little plaque or calculus is present. However, they do
present with evidence of subgingival plaque accumulation, both tissue associated and toothassociated plaque.

Bone loss is 3 to 4 times faster than adult periodontitis

Not be a single disease entity:

Caused by actinobacillus actinomycetemcomitans and bacteroids like organisms.

Neutrophil defects

Abnormalities in peripheral blood neutrophil (polymorphonuclear leukocyte) chemotaxis and

monocyte chemotaxis.

Anomalies of phagocytosis, bacterial activity, leukotriene B4 generation, and other defects

Hereditary basis for LAP; some believe the mode of transmission is autosomal recessive, but others
have provided evidence that the pattern is typical of an X-linked dominant mode.

GENERALIZED AGGRESSIVE
PERIODONTITIS
Seen at or around puberty in older juveniles and young adults

Affects the entire periodontium of the dentition

Caused by nonmotile, facultative, anaerobic, gram negative rod P.

gingivalis

Neutrophils in GAP patients have suppressed chemotaxis. Individuals

with GAP exhibit marked periodontal inammation and have heavy
accumulations of plaque
and calculus.

TREATMENT OF AGGRESSIVE
Successful treatment of aggressive periodontitis depends on early diagnosis,
PERIODONTITIS
use of antibiotics against the infecting microorganisms, and provision of an
infection-free
environment for healing.

Treatment of aggressive periodontitis, both the localized and generalized types

(LAP and GAP), includes surgery and the use of tetracyclines (sometimes in
combination with metronidazole).

In patients with LAP : a 2-week course of doxycycline hyclate 100 mg per day +
Surgical removal of infected crevicular epithelium and dbridement of root
surfaces during surgery

Keyes technique LAP: meticulous scaling and root planing of all teeth, with
concomitant irrigation to probing depth of saturated inorganic salt solutions and
1% chloramine T + systemic tetracycline (1 g per day) for 14 days (patients 12
years of age and older) + daily application of a paste of sodium bicarbonate and
3% hydrogen peroxide and inorganic salt irrigations.

Treatment of GAP is often less predictable. Alternative antibiotics directed at the

specific pathogenic ora may be required when there is no response to
traditional therapies. The multidisciplinary approach combines clinical