Gingival &

Periodontal
diseases in Children
Dr.G.Thiruvenkadam
Post Graduate
Dept of Pediatric & Preventive Dentistry

Presentation outline
Introduction
Anatomy
Differences between
Gingival diseases
Periodontal diseases

conclusion

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Introduction
Paediatric periodontics is the science that deals with the
upkeep and maintenance of periodontium in primary, mixed
and early permanent dentition.
The periodontium comprises gingiva, periodontal ligament,
cementum and alveolar bone.
The gingiva comprises attached gingiva, marginal gingiva and
interdental papilla.

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Anatomy of periodontium
Pert around
Odontos-teeth
Periodontium the attachment apparatus
Oral mucosa
Masticatory
Gingiva
Hard palate

Specialized
Dorsum of tongue

Lining

Gingiva
Free
Attached
Free gingival groove
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PDL soft, richly vascular and cellular connective tissue

which surrounds the roots of the teeth and joins the root
cementum
Situated between root cementum and lamina dura or the
alveolar bone proper
Hour glass shape, narrow at the midroot level
Width 0.25 mm(0.2-0.4)
The tooth is joined to the bone by bundles of collagen fibres
Alveolar crest fibres
Horizontal fibres
Oblique fibres
Apical fibres

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Cementum
Specialized mineralized tissue
Features common with bone tissue
No blood or lymph vessels, no innervations, no remodelling, but
continuing deposition throughout life
The portion of the principal fibres of the PDL which are embedded in
root cementum and alveolar bone proper is known as the sharpeys
fibres

Alveolar bone
Alveolar bone proper
Alveolar process/Pars alveolaris

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The periodontium of the primary dentition varies anatomically

and microscopically from that of the permanent dentition. The
aspects of clinical significance are as follows:
Anatomic variations in the periodontium of primary and permanent
dentition
Significant gingival features in primary dentition

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Anatomic Variation in the Periodontium of Primary

and Permanent Teeth

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SIGNIFICANT GINGIVAL VARIATIONS IN PRIMARY

DENTITION

Interdental gingival architecture:

The interdental gingiva is broad buccolingually and narrower
mesiodistally in primary dentition.
This interdental gingival architecture demands precise proximal
restorations where minor aberrations in proximal box contour can lead
to overhanging restoration.

Free gingival margin:

The free gingival margin in primary dentition is thick and rounded.
This is in accordance with the cervical bulge and the marked
constriction of the primary tooth at the cervix

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Retractable marginal gingiva:

The marginal gingiva is retractable around the primary tooth.
This makes the area more cleansable leaving very less chances for food
entrapment. Hence, gingival abscesses are rare in children.

Interdental clefts:
They are gingival clefts in the inter-radicular region underlying the
saddle area and are more common in primary dentition

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Retrocuspid papillae:
It is a sessile, elevated, well-circumscribed, soft mucosal nodule, first
described by Hirshfeld.
It is found in the lingual gingiva of the mandibular cuspids, in between
the free gingival margin and the mucogingival junction.
It is usually found bilaterally.
This structure is exceedingly common in primary dentition with as high
as 99% prevalence in the children of age group 816.
It regresses with age and needs no intervention as it is considered a
normal anatomic entity.

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Stippling:
It represents the functional adaptation of the gingiva to the masticatory
strain indulged on it.
Stippling is considered as a sign of healthy gingiva.
It is absent in infants and begins to appear at the age of 5 years.
It is reported to be found in 35% of children with peak prevalence
between 5 and 13 years. Stippling increases in adulthood and
progressively declines at old age.

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Absence of col:
Col is a parakeratinised or non-keratinised area beneath the interdental
gingiva.
It is a tent-shaped region, most susceptible to infection.
The col is absent in primary dentition.
This is considered as one of the reasons why periodontal diseases are
highly uncommon in primary dentition.

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Factors related to limited involvement of

periodontal diseases in children
Greater metabolic activity in children
Anabolism greater than catabolism( Robinson, 1951; Kelsten, 1955)
Offer greater resistance to periodontium and concurrent repair

Oral flora is different

Late establishment of spirochetes and bacteroids
Associated with gingivitis( deArugo, 1964; Maltais et al, 1978)
Absence of heme and alpha 2 globulin in gingival sulcus( Socransky
and Manganiello, 1971)

Lower irritation potential of the plaque

Mackler and Crawford, 1973; withheld oral hygiene practices for the
preschoolers for 27 days; no increase in degree of gingivitis
Direct contradiction to the findings of a similar study in adults( Loe et
al, 1965)
Cox et al, 1074 found that healthy preschool children with a plaque
index four times that of adults had only one fourth the gingival index.

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Reasons for delayed development of

gingivitis
Slight decrease in the leucocytic migratory rate in children
(Cox et al, Longhurst et al ,1977)
Lack of antibody or cellular hypersensitivity
Low levels of Ig specific for plaque bacteria

Less gingival permeability to bacterial antigen

Vascular inflammatory response is retarded in children

Decreased amount of gingival exudates and bleeding found in
children( Matson, 1978)

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The various conditions involving the gingiva of primary

dentition are as follows:
Physiological gingival changes with tooth eruption
Simple gingivitis
Gingival enlargement
Chronic inflammatory enlargement
Drug-induced enlargement
Conditioned enlargement
Puberty gingivitis
Scorbutic gingivitis
Plasma cell gingivitis

Idiopathic enlargement
Combined enlargement

Viral and bacterial infections

Cysts and reactive lesions
Neoplasm
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Physiological gingival
changes with tooth eruption

Significant changes occur in the gingiva during the eruption of

permanent teeth.
Normally, before the eruption of a permanent tooth, the
gingiva exhibits a bulge.
The mucosa is pink or blanched and firm corresponding to the bulbous
crown of the erupting tooth.

A prominent marginal gingiva commonly surrounds an

actively erupting tooth.

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This prominence of the marginal gingiva is called preeruptive bulge.

It is caused by the prominent height of contour of the erupting tooth
and mild inflammation due to mastication.

There are two significant conditions involving the gingiva

during eruption of teeth.
Eruption cyst
Pericoronitis.

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Eruption cyst

Occasionally, bluish discolouration is seen on the gingiva over

an erupting tooth
An eruption cyst implies that the erupting tooth is obstructed
partially or totally by some pathology.
It is associated with over-retained primary teeth and delayed
eruption of the permanent tooth.
Eruption cyst is common in the permanent first molar region.

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It also occurs in the regions of succedaneous teeth whose

predecessors have been lost prematurely, commonly
mandibular permanent incisors.
The eruption cyst may also be filled with blood.
If so, it manifests as a dark blue or dark red gingival enlargement on the
crest of the ridge.

The eruption cyst either resolves spontaneously or requires

marsupialisation as the mode of intervention.

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Pericoronitis

Pericoronitis is the acute inflammation of the gingiva around

an erupting tooth.
It is more common in the first permanent molar region.
It manifests as a fleshy gingival flap over an erupting tooth,
which is tender and has an increased tendency to bleed.
Referred as operculum, which attracts the food debris inflammation and infection
Regional lymphadenopathy, fever, trismus
Trt- antibiotics, irrigation and excision

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Management of pericoronitis
Pericoronitis

1. Deep subgingival scaling under antibiotic coverage

2. Amoxicillin 2040 mg/kg in three divided doses
3. Metronidazole 5 mg/kg thrice a day

Review after a week

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Lesion regresses

Persisting pericoronal flap

No further treatment required

Oral hygiene to be maintained

Operculectomyperformed

Simple gingivitis

Simple gingivitis or gingivitis is a chronic inflammatory

involvement of the gingival tissues with no apical migration of
junctional epithelium(loss of gingival attachment).
It is the result of the response of the gingival tissue to the
plaque microbiota at and below the gingival margin.
The marginal gingiva and the interdental papilla are almost
always involved in simple gingivitis.
Prevalence increases from 50% in 45 years and goes up to
100% at puberty and declines thereafter.
Gingivitis peaks at 1112 years in girls and 1113 years in
boys.

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Clinically:
It first appears on the marginal gingiva
Occasionally extends to the attached gingiva.
The gingival tissues :
Become red and swollen
Bleed upon probing or brushing as the conditions worsens.

Etiology
Irritating factors: plaque, material alba, food debris, calculus
Malocclusion
Habits: mouth breathing, tongue thrusting
Eruption of teeth

Treatment
Oral prophylasxis
Oral hygiene instructions
Chlorhexidine mouthwash
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Gingival enlargements
Gingival enlargement implies an overgrowth of the gingiva
that alters its size, contour and coherency of architecture
corresponding to the cervical line of the associated tooth.
Chronic inflammatory enlargement: This arises on untreated, longstanding simple gingivitis.
Drug-induced enlargement: This may be induced with the chronic use
of certain drugs.
Conditioned enlargement: This arises during conditions such as puberty
and vitamin deficiency.
Idiopathic enlargement: This is a non-inflammatory type of gingival
enlargement.

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Drug induced gingival enlargements

Gingival enlargement may be induced due to chronic use of
certain systemic medications.
The induced enlargement is non-inflammatory in nature.

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Clinical manifestations
Appears within 1-3 months after initiation of treatment with
the associated medications
The growth starts as a painless, beadlike enlargement of the
interdental papilla, and extends to the facial and lingual
gingival margins.
As the condition progresses, the marginal and papillary
enlargements unite; they may develop into a massive tissue
fold covering a considerable portion of the crowns
When uncomplicated by inflammation; the lesion is
mulberry-shaped, firm, pale pink, and resilient; with a
minutely lobulated surface and no tendency to bleed.
The enlargement is usually throughout the mouth, but is more
severe in the maxillary and mandibular anterior regions
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Puberty gingivitis

A distinct, chronic inflammatory type of gingival enlargement

is demonstrated in circumpubertal adolescents.
Gingiva is the target tissue for the steroid hormones
Estrogen affects salivary peroxidases, reduces redox potential(Kimura
et al, 1983)
Estrogen has stimulatory effects on metabolism of collagen and
angiogenesis(Sultan et al, 1986)
The high level of circulating corticosteroid hormones, during prepubescence or pubescence, increases the vascular permeability of the
gingiva and alters its pattern of microbial interaction(Soory, 2000)

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The prevalence of certain periodontal pathogens during

puberty may have direct association with the hormones present
and their utilization by selected pathogens
P.intermedia is able to substitute progesterone and estrogen for vitamin
K as an essential nutrient (Kornman & Loesche, 1979)

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Scorbutic Gingivitis
Scorbutic gingivitis arises in response to scurvy, the nutritional
deficiency of vitamin C in children.
In vitamin C deficiency, there is enhanced capillary fragility
with notable degeneration of capillaries.
The endothelium of the capillaries swells and vessel walls
become weakened, porous and haemorrhagic.
Features:
Involving marginal tissues & papillae
Severe pain
Spontaneous hemorrhage

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Treatment
Nutritional supplements: 250300 mg of vitamin C should be taken as
an oral daily dose.
The child should be motivated to consume foods rich in vitamin C such
as citrus fruits and citrus fruit juices.
Oral prophylaxis: This is performed in multiple visits as the gingiva
bleeds extensively.
On completion of oral prophylaxis, strict oral hygiene practices should
be advocated

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Acute gingival infections

Herpes Simplex Virus Infection
Acute herpetic gingivostomatitis
Primary infection occurs in a child under 6 y/o
99% are subclinical
Active symptoms: fiery red gingiva, malaise, irritability, headache, pain
when eating
Run a course of 10~14 days
Characteristic oral finding
Vesicles(yellow/white liquid-filled)
Ulcers (painful, 1~3mm) + whitish gray membrane

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Treatment for AHGS

Antiviral therapy
Systemic acyclovir 1530 mg/kg body weight in five divided doses for
a week is the antiviral regime for acute herpetic gingivostomatitis.
Topical 5% acyclovir ointment is ideal as a topical antiviral drug.

Symptomatic therapy
Topical local anaesthetics, such as 4% lignocaine with choline
salicylate, obtain good local anaesthesia and can be advocated for about
six times a day.
Rehydration of the child with plenty of fluids.

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Necrotizing ulcerative gingivitis

Necrotising ulcerative gingivitis is a bacterial infection caused by
Borrelia vincentii and Fusiform bacillus.
It is also referred to as a fusospirochetal infection.
This lesion usually presents in the 612 years age group and is
associated with poor oral hygiene.
The clinical manifestations are limited to the marginal gingival and
interdental papilla
The marginal gingival exhibits zones of redness and inflammation,
bleeding tendency, tenderness and necrosis.
The interdental papilla exhibits punched lesions depicting necrosis
of tissue.
The necrosed areas are covered by a pseudo-membrane.
Fetid odour (necrosis), general malaise and loss of appetite are other
symptoms.
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Zones of NUG(Listgarten, 1965)

Bacterial zone
Neutrophil rich zone
Necrotic zone
Zone of spirochetal infilteration

Treatment
Oral hygiene
Debridement mainstay of treatment
Systemic antimicrobial therapy penicillins and nitroimidazoles
Changes in architecture surgical correction to facilitate plaque control

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Neoplasms
Congenital gaint cell epulis
Soft, pedunculated, benign outgrowth of the gingiva, most commonly
found on the crest of the alveolar ridge
It is commoner in newborn girls and three times more common in the
maxilla.
The anterior alveolar ridge is a more common site than the posterior
alveolar ridge.
It may vary from a few millimetres to 9 cm (largest size reported) in
size
Treatment: surgical excision

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Peripheral ossifying fibroma

It is often associated with trauma or local irritants such as subgingival
plaque and calculi, dental appliances and poor quality dental
restorations.
High degree of cellularity usually exhibiting intralesional bone
formation, cementum- like material occasionally and dystrophic
calcification rarely.
POF is odontogenic in origin and is derived from the periodontal
ligament and it occurs only on the gingiva

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Some important periodontal pathogens

World workshop of Periodontology, 1996
Actinobacillus actinomycetemcomitans
Porphyromonas gingivalis
Bacteroids forsythus

A. actinomycetemcomitans
Gram negative, small, non-motile, rod shaped
Major pathogen in aggressive periodontitis

P.gingivalis
Gram negative, non-motile, coccal to short rod shaped, anaerobic
Most commonly seen in chronic periodontitis

B.forsythus
Gram negative, spindle shaped, anaerobic
Higher number in sites of destructive periodontal disease or periodontal
abscess and in active periodontal diseases

Other species are Spirochetes, Prevotella intermedia, Fusobacterium

nucleatum, Campylobacter rectus, Eikenella corrodens
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Mechanism of pathogenecity
Steps
Attachment adhesins
Coaggregation
Multiplication
Interbacterial relationshops
Overcoming of host defenses
Invasion
Tissue damage virulence

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Prepubertal periodontitis
Localised aggressive periodontitis
Generalised aggressive periodontitis
Periodontitis in systemic diseasesDiabetes mellitus
Downs syndrome
AIDS
Hypophosphatasia
PapillonLefvre syndrome
Leukaemia
Immune-compromised states

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Prepubertal periodontitis
Page et al, 1983 classified into two types
Localized
Generalized

Localised
Onset of 4 years of age
Bone loss is rapid
Functional abnormalities either in neutrophil chemotaxis or in
monocytes
Significant plaque accumulation and gingival inflammation is absent
Affected sites harbor elevated % of Actinobacillus
actinomycetemcomitans, Provotella intermedia and Porphyromonas
gingivalis
Progression of the disease is altered by local debridement, antibiotic
therapy, improved oral hygiene
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Generalised
Occurs in children with persisitent
infection and delayed wound healing
Alveolar bone destruction is more
rapid
Severe gingival inflammation and
clefting
Functional abnormalities occurs in
both neutrophils and monocytes
Refractory to antibiotic therapy
Extraction of affected teeth only
treatment

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Aggressive periodontitis
Comprises a rare, often severe, rapidly progressive forms of
periodontitis
Manifests at early age
Lang et al,1999, major common features
Non contributory medical history
Rapid attachment loss and bone destruction
Familial aggregation of cases

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LAP
Also called as Juvenile periodontitis
Circumpubertal onset
Localised first molar/incisor with interproximal attachment
loss
Arc shaped bone loss
Involves not more than two teeth other than molars and
incisors
Robust serum antibody response to infective agents

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Generalised aggressive periodontitis

Affects less than 30 years of age
Generalised interproximal attachment loss
Involves atleast three permanent teeth other than molars and
incisors
Pronounced episodic nature of the destruction of attachment
and alveolar bone
Poor serum antibody response to infecting agents

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Treatment
Oral hygiene instructions
Reinforcement and evaluation of the patients plaque control
Supragingival and subgingival scaling and root planing
Control of other local factors
Occlusal therapy, if necessary
Periodontal surgery, if necessary
Periodontal maintenance
A general medical evaluation may rule out underlying systemic
diseases.
Adjunctive antimicrobial therapy, as well as microbial identification
and antibiotic testing, should be considered.
When the primary teeth are affected, the eruption of the permanent
teeth and their attachment levels should be monitored.
Finally, evaluation and counseling of family members is wise, as the
disease can be familial
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Systemic disorders associated with

periodontitis AAP,1999
Associated hematological disorders
Acquired neutropenia
Leukemias
Other sickle cell, aplastic anaemias, thalassemias

Associated with genetic disorders

Familial and cyclic neutropenia
Down syndrome
LADS Leukocyte Adhesion Deficiency Syndrome
PLS Papillon Lefevre Syndrome
Histiocytosis syndromes
Glycogen storage diseases
Infantile genetic agranulocytosis
Cohen syndrome

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Cyclic neutropenias
AD
Rhythmic reduction of PMN in 21 day cycles
Severe ulcerative gingivitis
Alveolar bone loss
Both primary and permanent dentition

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Leukemias
Abnormal and uncontrolled
proliferation of the immature
leucocytes
Usually agranulocytes
Lymphocytic and monocytic

Gingival enlargement and

ulceration leucocytic
infilteration
Also due to chemotherapeutic
agents

Leukemia
Immature leucocytes
Gingival infilteration
Thinning of lamina dura
Destruction of periodontal
ligaments and fibres

Tooth migration

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Hypophosphatasia
AR
Low serum alkaline phosphotase
Increased urine phosphoethanolamine levels
Premature mobility and loss of primary teeth
Incisors more common than molars
Higher prevalence in uniradicular primary teeth

Acementogenesis, dentinal dysplasia, enlarged pulp chambers

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Papillon LeFevre syndrome

AR
Hart et al, 1998, chromosome 11q14-q21
Precocious periodontitis
During eruption- normal
By 2 years of age Gingival bleeding, hyperkeratosis of palms
and soles
At 2.5 years, higher mobility, severe horizontal bone loss

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Histiocytosis X
A nonlipid reticuloendotheliosis marked by multiple hard and
soft tissue lesions containing histiocytes and eosionphils
Three clinical entities
Letterer-Siwe disease severe and in infants
Hand-Schuller Christian disease children > 3 years and involve
mainly bones
Eosinophilic granuloma- benign, older children

Oral manifestations occur in 1/3 of patients

Necrotic gingivitis, bone loss in bifurcation of molars
Radiolucent lesions of mandible and skull
Floating tooth appearance

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Acrodynia
Pinks or Swifts disease
Excessive exposure to mercury
Desquamation of skin, glossitis
Premature eruption and exfoliation of teeth

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Vitamin D resistant rickets

X linked dominant
Also called as refractory rickets and low phosphate diabetes
A number of isolated renal tubular defects, associated with an
inability to reabsorb certain metabolites such as water,
phosphates, calcium and potassium
Marked effects on teeth and supporting structures
Globular hypocalcified dentin clefts and tubular defects in
pulp horn regions pulp horns are high and
elongatedinvasion of microbes without destruction to
tubular matrix periapical involvement of normally appearing
teethdevelopment of multiple gingival fistulas
Abnormal cementum, lamina dura is absent, alveolar bone
pattern is abnormal
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Juvenile Diabetes mellitus

sixth complication of diabetes
Gingiva:
Pain and inflammation
Greater tendency to bleeding
Enlarged gingiva
Sessile, pedunculated gingival polyps
Painful abscess

PDL diseases
Fulminating periodontitis with periodontal abscess formation
Periodontal breakdown, extensive bone loss, increased tooth mobility,
widening of PDL, suppuration and abscess formation

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Down syndrome
Mongolism, trisomy 21
Mental deficiency and growth retardation
Although plaque and calculus are present and oral hygiene is
poor, the severity of periodontal destruction exceeds that
explain by local factors alone
Deep periodontal pockets with substantial paque accumulation,
moderate gingivitis
Findings are generalised and more severe in lower anterior
region
Marked recession of gingiva, associated with high frenum
attachment

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Two factors have been proposed for high prevalence and

increased severity of periodontitis in Down syndrome patients
A reduced resistance to infections because of poor circulation,
especially in regions of terminal vascularisation such as gingival tissue
Defect in T cell maturation and PMN chemotaxis

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LADS
AR, single gene defect
Impaired adhesion of neutrophils to the vessel walls due to restricted
expression at the cell surface
The prominent clinical feature of these patients is recurrent bacterial
infections, primarily localised to skin and mucosal surfaces.
Severe gingivitis and periodontitis are major features among all
patients who survive infancy
Acute inflammation and proliferation of gingiva
Rapid destruction of bone
Symptoms appear during or immediately after eruption of the primary teeth

The absence of pus formation at the sites of infection is one of the

hallmarks of LAD
Absence of neutrophils in the gingival tissue have been noted

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Chediak-Higashi syndrome
Characterized by recurrent bacterial infections and rapidly
destructive periodontitis
Appears soon after birth or in children younger than 5 years
AR disorder characterized by abnormal intracellular protein
transport defective leucocyte function(phagocytosis)
Decrease in phagocytosis results in recurrent pyogenic infections,
partial albinism and peripheral neuropathy

Treatment
There is no specific treatment for ChdiakHigashi syndrome.
Bone marrow transplants appear to have been successful in several
patients.
Infections are treated with antibiotics and abscesses are surgically
drained when appropriate.
Vitamin C therapy has improved immune function and clotting in some
patients
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Conclusion
Children and adolescents are subject to several gingival and
periodontal diseases.
Although there is a much lower prevalence of destructive
periodontal diseases in children than in adults, children can
develop severe forms of periodontitis.
Current modalities for managing periodontal diseases of
children and adolescents may include antibiotic therapy in
combination with non-surgical and/or surgical therapy.
Since early diagnosis ensures the greatest chance for
successful treatment, it is important that children receive a
periodontal examination as part of their routine dental visits

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