GINGIVITIS AND PERIODONTAL DISEASES IN CHILDREN

A Presentation by: Shruti Goel

MODERATED BY: Dr Harpreet Grewal Dr Mridula Goswamy Dr Gyanendra

Dr Meera Dr Ashok

PERIODONTAL DISEASESIN CHILDREN

FEATURES SEEN IN CHILDREN

Greater sulcus depth (1.4-

2.1mm)

Free

gingiva –

more

thicker &

rounded.

Periodont

al space

is wid

er

Alveolar

bone is m

ore calcified

& vascular.

Thin lamina dura is present

INTRODUCTION Inflammatory Disease of gingiva and

deeper tissues of periodontium Characterized by pocket formation and

destruction of supporting alveolar bone. Distance of alveolar crest to CEJ

2-3 mm= questionable bone loss>3 mm= definite bone loss

In preschool children- no recession, gingival erythema and edema (Delaney)

Periodontitis

Pubertal

Juvenile

Rapidly Progressing

Adult

EARLY-ONSET PERIODONTITIS Used as a generic term to describe a

heterogeneous group of periodontal diseases occuring in young individuals who are otherwise healthy.

Early-Onset

Juvenile

Localized

Generalized

Prepubertal

Early-Onset

Juvenile

Localized

Generalized

Prepubertal

JUVENILE PERIODONTITIS

Juvenile periodontitis

Localized “severe attachment and bone loss

around the first molars and incisors (but not involving more than two additional non first molar/incisor teeth), which occurs between the

ages of 12 to 26 years.”

Generalized“severe attachment and

bone loss involving more than two teeth in addition to first molar/incisor teeth.”

Juvenile Periodontitis

Acute Progressi

ve

Fairly Generali

zed

Chronic Slowly

Progressive

JP

Occuring in healthy individual

Associated with a variety of diseases of other systems

ETIOPATHOGENESIS

Bacteria

(certain kind)

•Actinobacillus actinomycetemcomitans

Host response

•Impaired PMNs (phagocytosis, chemotaxis and decreased receptors)

Possibly

genes

•may be AD inheritance

ETIOPATOGENESISPMN Dysfunction

Susceptibility to infection

A. Actinomycetemcomitans

Antibody

Local PMN and Macrophage destruction

Accelerated Disease

Neutralisation

Serum Amplification leukotoxins

CLINICAL FEATURESLoss of attachment and alveolar bone around permanent incisors and first molars

Detected at ages 10-15

Diagnosis made when 3 sites have CAL of 5mm or greater

Familial Aggregation

Lack of clinical inflammation despite the presence of deep pockets

Premature and excessive mobility of affected teeth

Regional lymphadenopathy

CLINICAL FEATURESDistolabial migration of maxillary incisors with diastema formation

Apparent increase in the size of clinical crown

Rapid progression- Rate of bone loss is 3-4 times more than typical periodontitis.

Denuded root surfaces become sensitive to thermal and tactile stimuli.

Deep, dull radiating pain

Periodontal abscesses

Small amount of plaque, calculus rarely

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RADIOGRAPHIC FINDINGS

Vertical

alveolar

bone loss around the first

molars and inciso

rs.

Arc shape

d bone loss

extending from the

distal surface of the

second

premolar

to the mesia

l surface of the first

molar.

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Arc like bone loss

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MICROBIOLOGY

A. actino-

mycetem-

comitans

Gram negative

anaerobes

Capnocyto-phaga

A.A

Gram negative, facultative anaerobic, coccobacillus

Makes leukotoxin kills macrophages

Why is A.a the culprit? None or low levels of A.a found at non

diseased sites Extermination of A.a = Clinical

Success Presence of A.a after treatment

resulted in progressive attachment loss

IMMUNOLOGY

Increased frequency and

severity of bacterial infections

Defective production or

function of circulating neutrophils

WHAT HAPPENS IN THE PROGRESSION? Lost Teeth:

Over a 6 year period Untreated 43% lose teeth

35% cases of untreated LAP lead to Generalized Aggressive Periodontitis

JUVENILE PERIODONTITIS: ARTICLES “Five-year maintenance follow-up of early-onset periodontitis

patients.” J Clin Periodontol. 2003 Jun;30(6):562-72

Study:

25 patients with JP

Received Supportive Periodontal Therapy (SPT) for 5 year period SRP and Localized Antibiotic Placement

Average 12-13 sessions of SPT over the 5 year period

Improvements in pocket depths, clinical attachment loss and gingival index

However, 134 sites showed CAL greater than or equal to 2mm Bacteria most prevalent in these failures:

P. gingivalis T. denticola

Note: Confounded by smoking and stress

JUVENILE PERIODONTITIS: ARTICLES

“Actinobacillus actinomycetemcomitans as indicator for aggressive periodontitis by two analyzing strategies.” J Clin Periodontol. 2007 July;34(7):566-573

Study: 60 patients with JP or Chronic Periodontitis samples

taken of subgingival plaque using paper points Plaque analyzed for A.a, T. forsythensis, P. gingivalis

and T. denticola Higher levels of A.a in LAP versus Chronic

Periodontitis Lower levels of other pathogens in A.a versus Chronic

Periodontitis

JUVENILE PERIODONTITIS: ARTICLES “Comparative evaluation of surgical and conservative

treatment modalities of juvenile periodontitis patients.” Afr J Med Med Sci. 2001 Dec;30(4):313-8.

Study: 12 patients, 6 mon longitudinal study Split mouth tx:

1 side conservative 1 side surgical and antibiotic therapy Look at mobility and CAL Use SRP and systemic antibiotic use

“It was therefore concluded that surgical debridement with systemic administration of tetracycline is more effective than the conservative technique in the treatment of juvenile periodontitis, although both gave improvement”

DIFFERENTIAL DIAGNOSIS

Hypophosphatasia

Papillon-Lefevre

syndrome

Histiocytosis-X

Neutropenia

Cyclic Neutropenia

TREATMENT

Depends upon

EARLY DIAGNOSIS

HistoryClinical

Examination

Radiographic

Interpretation

DNA test kit• DMDx test kit

(Microdentex)• Aids in

• establishing the risk of JP

• confirms the response to antibiotic therapy

USE OF ANTIBIOTICS 2 week course of Doxycycline hyclate (1

g per day) Sometimes combined with

metronidazole Rationale- concentrations of

tetrracyclines achieved in GCF is 2-10 times greater than that in plasma

HOW TO PROVIDE INFECTION-FREE ENVIRONMENT FOR HEALING? Meticulous scaling and root planing Concomitant irrigation to probing depth

of saturated inorganic salts and 1% chloramine T.

Home care treatment : Daily application of a paste of sodium bicarbonate and 3% hydrogen peroxide and inorganic salt irrigations.

Early-Onset

Juvenile

Localized

Generalized

Prepubertal

PREPUBERTAL PERIODONTITIS

Prepubertal Periodontitis

Localized Generlized

LOCALIZED PREPUBERTAL PERIODONTITIS Localized attachment loss and alveolar bone loss only

in the primary dentition in an otherwise healthy individual

Etiology Abnormalities in host defences Extensive proximal caries facilitating plaque retention Familial

Clinical Features: Onset- around 4 yrs of age Abnormal probing depths with minor gingival inflammation,

rapid bone loss, and minimal to varying amounts of plaque Advanced stages show signs of gingival inflammation with

gingival crests and localized ulceration of gingival margin.

GENERALIZED PREPUBERTAL PERIODONTITIS: ETIOLOGY Occurs in families More common in females This suggests X-linked pattern of

inheritence Defect may also be acquired and might

have resulted from a inhibition of chemotaxis derived from periodontal bacteria

GENERALIZED PREPUBERTAL PERIODONTITIS: MICROBIOLOGY

A.a

P.ging

B.melaninP.intermedi

a

C.sputigena

F. nucleatum

GENERALIZED PREPUBERTAL PERIODONTITIS: CLINICAL FEATURES

Onset- during or soon after eruption of primary teeth

History of recurrent infections: otitis media, skin infections, URTIs

Severe gingival inflammation, generalized CAL, tooth mobility, rapid alveolar bone loss with premature exfoliation of teeth(by 3 yrs of age).

Initially gingiva is minorly inflamed with minimal plaque.

Chronic cases- clefting and pronounced recession with accute inflammation

PREPUBERTAL PERIODONTITIS: TREATMENT

Early Diagnosis

Consultation with physician to rule out systemic disease

Dental curettage

Root planing

Prophylaxis

OHI

Restoration of decayed teeth

Removal of primary teeth that have lost bony support

Use of antimicrobial rinses(chlorhex), and therapy with broad spectrum antibiotics (amoxycillin, tetracycline)

PAPPILON-LEFEVRE

SYNDROME(Precocious Periodontitis)

PAPILLON-LEFÈVRE SYNDROME First described by two French physicians, Papillon and

Lefèvre, in 1924 Prevalence of 1-4 cases per million persons Consanguinity between parents in 1/3 of cases Males and females are equally affected with no racial

predominance Rare genetic disorder Autosomal recessive

ETIOLOGYNeutrophil defects:•Decreased neutrophil chemotaxis and phagocytosis

Bacterial infection•A. actinomycetemcomitans

Natural killer cell defect: •Cytotoxicity

Endocrinopathy

Vitamin A deficiency

CLINICAL FEATURES

Hyperkeratosis

Precocious periodontal destruction with loss of both

dentitions

Ectopic intracranial calcifications

Skin Lesions• The palmoplantar

keratoderma typically has onset between the ages 1 to 4 years

• The sharply demarcated erythematous keratotic plaques may occur focally, but usually involve the entire surface of palms and soles resulting in foul-smelling odor Well-demarcated

psoriasiform plaque occur on elbows and knees, this may worsen in winter and be associated with painful fissures

ORAL LESIONSEarly onset of severe periodontitis •starts at the age 3 or 4 years.•Development and eruption of deciduous teeth proceeds normally•eruption is associated with gingival inflammation and rapid destruction of the periodontium. •unresponsive to traditional treatment modalities •primary dentition is exfoliated prematurely by age 4 to 5 years. •After exfoliation, the inflammation subsides and gingiva appears healthy. •In permanent dentition the process of gingivitis and periodontitis is repeated •Without treatment, most of the permanent teeth may also be lost by age 17. 

ECTOPIC INTRACRANIAL CALCIFICATIONSOf tentorium falx cerebri and choroid plexus

Low Hb

Radiographic features are characterized by generalized loss of alveolar bone, rapid bone loss.Incomplete root formationUnerupted teeth assume abnormal positions

Other Features

Marked predisposition for infections

PYOGENIC LIVER ABSCESS IN PLS

Pyogenic liver abscess is increasingly recognized as a complication of PLS because of impairment of the immune system.

The risk of pyogenic liver abscess should be kept in mind in evaluating these patients when they present with fever of unknown origin.

A course of antibiotics should be tried to control the active periodontitis in an effort to preserve the teeth and prevent bacteremia and subsequently pyogenic liver abscess.

The most common etiologic agent is S aureus, and most often a solitary abscess is found

PLS VS NON-SYNDROMIC PREPUBERTAL PERIODONTITIS

PLS NS-PPP

Cathepsin C gene mutation

2126CT substitution

1040AG substitution

Palmoplantar keratosis

Y N

Progressive periodontal disease

Y Y

Teeth effected Generalized Generalized or Localized

Patterns of familial transmission

AR AD and AR

PLS VS LJP

PLS LJP

CTSC gene defect Y N

A. a. Y Y

Reduced chemotaxis Y Y

PMN defect Y Y

Teeth effected Generalized Localized

DERMATOLOGIC TREATMENT

A multidisciplinary approach is important for the care of patients with PLS, skin manifestations are usually treated with emollients

Salicylic acid and urea may be added to enhance their effects

Oral retinoids including acitretin, etretinate, and isotretinoin are used in treatment of both the keratoderma and periodontitis associated with PLS

PERIODONTAL TREATMENT

PERIODONTAL TREATMENT Treatment may be more

beneficial if it is started during the eruption and maintained during the development of the permanent teeth

Therapy: aggressive local measures to control plaque including rigorous oral hygiene, chlorhexidine mouth rinses, frequent professional prophylaxis, and periodic appropriate antibiotic therapy needed for long-term maintenance

The periodontitis in PLS is usually difficult to control.

These patients often end up wearing dentures or and implant-supported prosthesis

HYPOPHOSPHATASIA

HYPOPHOSPHATASIA Initially recognized by Rathbun in 1948,

hypophosphatasia is a rare inborn error of metabolism caused by low activity of the tissue-nonspecific isoenzyme of alkaline phosphatase

ETIOLOGY Familial disorder of inborn error of

metabolism Autosomal recessive/ dominant

inheritance

CLINICAL FEATURES

Infantile Type

•Birth- 6 months

Childhood type

•6-14 months

Adult type

•Manifests during chilhood

CLINICAL FEATURES Abnormal

mineralization of bone and teeth

Premature exfoliation of primary teeth

Only the deciduous teeth are affected

DIAGNOSIS

Consistent clinical history

Physical Findings

Low serum alkalinase activity

TREATMENT Wide variety of treatments have been

attempted without a proven success Like oral phosphate supplements, i.v.

infusion of plasma etc.

HISTIOCYTOSIS X Reactive disorder in which

the proliferation of langerhans cells results from disturbances in immunoregulation

Langerhans cell is of marrow origin and is found in the epidermis.

Oral manifestations: Ulcerative necrotizing lesions

of the gingiva root exposure Increased mobility of teeth Halitosis Osteolytic areas of alveolar

bone in the radiographic examination giving the appearance of “floating teeth”

CYCLIC NEUTROPENIA Disappearance of neutrophils occurs

periodically, approx. every 3 weeks After 5-8 days,the neutrophils begin to

reappear Autosomal recessive trait Periodic symptoms- skin and ear infections Mucus membrane ulcerations, severe

stomatitis and profound neutropenia develop over a recurrent period of 14-24 days

Neutropenic conditions are usually accompanied by or slightly preceeded by monocytosis

CYCLIC NEUTROPENIA Attached, papillary and marginal gingiva

are enlarged, edematous and erythematous and bleed easily on a gentle provocation.

Antibiotics are ineffective and bone resorption progresses rapidly to the teeth.

During neutropenic stage periodontal disease and destruction occurs and during non neutropenic stage oral health returns.

CYCLIC NEUTROPENIA

CHRONIC PERIODONTITIS Caused by microbial plaque Attachment loss in initial

stage is 1-2 mm True periodontal pockets of 4-

5mm Incipient crestal alveolar

bone loss >0.5 mm Mesial and distal sites on first

molars and incisors most commonly affected

Slow progression

PERIODONTITIS IN DIABETES MELLITUS (TYPE 1) Incidence increases after puberty with

age Increased attachment loss and bone

loss in poorly controlled diabetes Increased susceptibility to infections Reduced wound healing Due to

Decreased neutrophil functionCollagen crosslinkingFormation of AGEs

PERIODONTITIS IN HIV/AIDS

Necrotizing ulcerative periodontal disease

Necrosis and loss of papillary and marginal gingiva and bone

Spontaneous gingival bleeding

Deep, aching pain May progress to cancrum oris

or noma in undernourished or debilitated individuals

PERIODONTITIS ASSOCIATED WITH SMOKING Increased attachment loss and bone

loss at an earlier age Characteristic periodontal changes

include Fibrotic gingiva Reduced gingival bleeding Anterior recession Maxillary palatal surfaces often more

severely affected Nicotine staining

Poorer response to periodontal treatment, maybe refractory periodontitis

Neutrophil function affected More susceptible to necrotizing

ulcerative gingivitis (NUG)

NECROTIZING PERIODONTAL DISEASE High level of spirochetes and P. intermedia

invasion of the tissues Factors that predispose children to NPD

include Viral infections including HIV Malnutrition Emotional stress Lack of sleep A variety of systematic diseases

Presence of interproximal necrosis and ulceration and rapid onset of gingival pain

Pts. may be febrile

Thank You

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