PERIODONTAL DISEASES IN CHILDREN

3. Anatomy of the periodontium in
children
Gingiva
Marginal gingiva
 For children,marginal gingival tissue around the primary
dentition are more highly vascular
 contain fewer connective tissue than tissues around the
permanent teeth.

4. Attached gingiva
 The width of attached gingival is less variable in the primary
dentition,
 there is less mucogingival problem in the primary dentition
Junctional epithelium
 There continue to be an apical shift when the teeth are fully
erupted.
 the gingival margins are frequently at different levels on adjacent
teeth that are at different stages of eruption.
 Sometimes it gives an erroneous appearance that gingival recession
has occurred around those teeth that have been in the mouth
longest.
 Stability is achieved at 12 years for 1 2 3 5 6, 16 years for the other
teeth.

5.  Periodontal ligament
 Periodontal ligament space is wider in children
 It is less fibrous and more vascular
 Cementum
 Thinner
 Alveolar bone
 Thinner cortical plates
 Larger marrow spaces
 Greater vascularity
 Fewer trabeculae

6. Gingival conditions
 Acute gingivitis
 Chronic gingivitis
 Gingival overgrowth
 Factitious gingivitis
 Mucogingival problems

7. Primary herpetic gingivostomatitis
Definition:
An acute infectious disease of the gingiva caused by the herpesvirus
Pathogeny:
 Herpes simplex viruses Herpes simplex viruses (HSVs)
 Two types exist: type 1 (HSV-1) and type 2 (HSV-2). Both are closely related but
differ in epidemiology
 Type-1 Gingivostomatitis
 Type-2 Genitalia
Transmission:
 HSV-1 is transmitted chiefly by contact with infected saliva
 Infected saliva from an adult or another child is the mode of infection.
 HSV-2 is transmitted sexually or from a mother's genital tract infection to her
newborn.

8. Prevalence:
 HSV infection appears to have increased worldwide in
the last 2 decades, making it a major public health
concern.
 Many primary infections are asymptomatic, Herpes
simplex infections are asymptomatic in as many as
80% of patients,
 Symptomatic infections may be characterized by
significant morbidity and recurrence.
Moreover, infections can cause life-threatening
complications, particularly in immunocompromised
hosts.

9. Clinical features:
Age:
 6 months to 3 years
Incubation period
 1 week
Prodrome:
 Febrile illness
 Headache, malaise, oral pain
 Cervical lymphadenopathy

10. Symptom
 Gingivitis:
 Gingivitis is the most striking feature,
 with markedly swollen, erythematous, friable gums
 Vesicular lesions:
 Vesicular lesions develop on oral mucosa ,lip and tongue
 can occur anywhere in the oral cavity,
 on the perioral skin,
 on the pharynx
 Diagnosis: According to Clinical features,History and age

11. Prognosis
 Oral lesions heal without scarring
Course:
 Acute disease lasts 5-7 days, and the symptoms
subside in 2 weeks.
 Viral shedding from the saliva may continue for 3
weeks or more.
 Adults also may develop acute gingivostomatitis,
 but it is less severe and is associated more often with a
posterior pharyngitis.

12.  Treatment:
 The availability of effective chemotherapy underscores that
the prompt recognition of the infection
 early initiation of therapy are of utmost importance in the
management of the disease.
 The goals of treatment are to make the patient comfortable
and to prevent secondary infections or worsening systemic
illness. It includes:

13. Pharmacotherapy
 Antiviral treatment
.
 Symptomatic treatment

14.  Antiviral treatment :
 Overall, medical treatment of HSV revolves around specific
antiviral treatment.
 Patients should be advised about the potential for
autoinoculation if they touch the herpetic lesion and then
touch a mucous membrane or an eye.
 Controlling autoinoculation can be a challenge if the patient
is a young child.

15. Symptomatic treatment
In situations in which constitutional effects such as fever
occur, symptomatic treatment can be used.
 Analgesics, such as acetaminophen, may make the patient
more comfortable.
 Aspirin should be avoided in pediatric patients because of the
possibility of Reye syndrome.
 Topical anesthetics and coating agents may make the patient
more comfortable and may aid in the consumption of food;
however, they do not speed healing.
 Appropriate wound care is needed, and treatment for
secondary bacterial skin infections may be required

16. Supporting treatment :
 Soft diet
 Be kept well hydrated:
 The patient should maintain fluid intake and a balanced diet
with the use of liquid food replacement if necessary
 Bed rest

17.  Warnings to parent:
 No school, day care etc.
 Children are highly contagious
 Sterilize eating and drinking utensils
 Disease is self-limiting; 10-14 days in duration

18. Acute necrotizing ulcerative
gingivitis(ANUG)
Aetiology:
 Broad anaerobic infection
 Causative organism: Fusiform bacteria , Spirochaete
 Other Gram-negative anaerobic organism
 Clinical features:
 Necrosis and ulceration
 Interdental papillae marginal gingival
 Covered by yellowish-grey pseudomembranous slough,
 Acute stage enters a chronic phase after 5-7days.
 Recurrence of the acute condition is inevitable
Pre-existing gingivitis
Distinctive halitosis

19. Treatment
 Intense oral hygiene
 Oxidant: hydrogen peroxide
 Mechanical debridement
 Metronidazole

20. Chronic gingivitis
 Chronic gingivitis is a common condition.Untreated, gingivitis may
progress to gum disease or periodontal disease.
 Gingivitis is painless in the early stages, but may lead to bleeding gums
and other oral problems.
 Bleeding gums are only one sign of gingivitis.
 Gums become red and swollen,
 teeth may become loose or may eventually fall out.

21. Prevalence:
increases steadily between the ages of 5 and 9 years, peaks at 11 years and
decrease slightly with age to 15 years.
Etiology:
Closely associated with the amount of plaque, debris and calculus
present.
 Eruptive gingivitis
 Filth gingivtis
 Crowding gingivtis
 Puberty gingivitis
 Catarrh gingivitis

22. scurvy
People at risk of scurvy include:
 People with chronic malnutrition or those that eat less
than 2 servings of fruits/vegetables per day
 Alcoholics
 Elderly
 Men who live alone (bachelor or widower scurvy)
 Children
 People on peculiar diets or food fads
 People with other medical conditions that may prevent the
intake and/or absorption of vitamin C
 Dialysis patients
 Malabsorption disorders
 Severe dyspepsia. [2]+[1]

23. Signs & symptoms
 Symptoms of scurvy generally develop after at least 3
months of severe or total vitamin C deficiency, they
includes:
 Weakness & fatigue
 Bruising easily & bleeding from weakening blood
vessel, connective tissue & bones due to collagen loss.
 Hair, teeth loss & gingivitis .
 Infants may be irritable, have pain when they
move, and lose their appetite. Infants do not gain
weight as they normally do.
 In infants and children, bone growth is impaired, and
bleeding and anemia may occur.

24. Oral manifestations
• gums may swell and become red, soft and
spongy. Any slight friction may cause the
gums to bleed.
• Often this results in poor oral hygiene
and dental diseases
• The gum findings are most
• striking in the interdental and marginal
gingiva, which
• become red, smooth, swollen, and shiny.
• Later thegums appear
purplish, sometimes even black and
• necrotic5,

25. Papillon Lefevre Syndrome
 -Papillon-Lefevre Syndrome
 (Palmoplantar Keratoderma with
Periodontosis)
 -Inherited as an autosomal recessive trait
 -Mutation of the gene that produces the
enzyme Cathespin C.
 -Greater frequency in consanguineous
offspring

26. Clinical features
 -Children are born looking completely normal. They may have redness on
palms of hands and soles of feet.
 -Teeth erupt in normal sequence, position, and time.
 -At age 1, when primary teeth starting to erupt, the gum tissue is severely
inflamed and generalized aggressive periodontitis accompany the teeth.
 -By age 4, the child has lost all of there primary dentition.
 -Gingival tissue in mouth goes back to healthy & normal.
 -Eruption of the permanent dentition begins at normal age and in normal
sequence
 -Patient will loose their permanent teeth and be completely edentulous by age 14-
17

27. Clinical Features

28. Papillon-Lefevre Syndrome

29. Radiographic Features
teeth seem to be “floating on air”
-severe bone loss

30. Eruptive gingivitis
Cause：
 Trauma of gingiva
 Debris and food residue
Clinical feature:
Site:
Primary teeth and the 1st permanent molar
Treatment：
 Oral hygiene

31. Filth gingivtis
 Clinical feature:
 Age: 3Y~5Y
 Site：Buccal, Papi
 Symptom：redness, bleeding
 Treatment:
 1）Local cleaning, antiinflection
 2）Oral hygiene

32. Puberty gingivitis
 Cause:
 Increase of sex hormones in circulating levels
*sex hormones :
Oestrogen
 Increases the cellularity of tissues and provides suitable growth
condition for species associated with established gingivitis
Progesterone
Increases the permeability of the gingival vasculature
Clinical features：
 Good oral hygiene,
 gum tends to bleed and hyperplasia
 Bad oral hygiene

33. Catarrh gingivitis
 Cause
 The infection of hemolytic streptococcus
 Clinical features：
Oral lesion
 soft and hematose gum,
 no vesicles or ulcers
Systemic reaction：
 fever，
 headache，
 myalgia,
 arthralgia
 Treatment：
 Local: Rinse

34. Crowding gingivitis
 Symptom:
 Redness and thickness
 Treatment:
 Oral hygiene
 Orthodontic treatment

35. Factitious gingivitis
Minor form
 Etiology: Rubbing or picking the gingiva using the fingernail, or from abrasive
foods
 Management: correct the habit and remove the source of irritation
Major form
 The injuries are more severe and widespread ,
 can involve the deeper periodontal tissues.
 Other areas of the mouth such as the lips and tongue may be involved.
 Extraoral injuries may be found on the scalp, limbs or face.
 Management
 A Dressing and protection of oral wounds
 B No lying with dentists
 C Psychological or psychiatric consultation

36. Riga–Fede disease
 Riga–Fede disease is an oral condition
found, ararely, in newborns
 that manifests as an ulceration on the ventral surface
of the tongue or on the inner surface of the lower lip.
 It is caused bytrauma to the soft tissue from
erupted baby teeth.[1]
 It can be described as a sublingual traumatic
ulceration.
 Although it begins as an ulceration, it may progress to
a large fibrous mass with repeated trauma

38. Drug-induced gingival overgrowth
 The clinical changes of drug-induced overgrowth are very similar irrespective of
the drug involved.
 The first signs of changes are seen after 3-4months of drug administration.
 Progress: The interdental papilla become nodular before enlarging more
diffusely to encroach upon the labial tissue
 Site:The anterior part is most severely and frequently involved
Sypmtom:
 with a good standard of oral hygiene,
 overgrowth gingiva is pink,firm and stippled,
 When there is a pre-exiting gingivitis the enlarged tissues compromise an
already poor standard of plaque control.the gingiva then exhibit the classical
signs of gingivitis

39. Management
 A strict programme of oral hygiene instruction, scaling and
polishing must be implemented.
 Severe cases of gingival overgrowth inevitably need to be
surgically excised and then recontoured to procedure an
architecture that allows adequate access for cleaning
 A follow-up programe is essential to ensure a high standard
of plaque control and to detect any recurrence of the
overgrowth.
 To modify or change the anticonvulsant therapy if
phenytion-induced overgrowth is refractory
 Indefinite oral care if there is no alternative.

40. Periodontal complications of
orthodontic treatment
 Gingivitis
 Gingival overgrowth
 Attachment and bone loss
 Gingival recession
 Trauma

41. Early-onset aggressive periodontal
disease
Generalized form
 Gingiva:
 fiery red,swollen,and haemorrhagic
 Tissue:
 hyperplastic with granular or nodularproliferation
 Gross deposits of plaque
 Progress: extremely rapidly, primary teeth loss:3-4 years
 Bone loss: may be restricted to one arch

42.  Localized form
 A Progresses more slowly
 B Bone loss affects only incisor-molar teeth
 C Plaque levels are low
 Treatment
 A Intense oral hygiene at frequent intervals
 B Antibiotic
 C Extraction of the teeth

43. CONCLUSION
 Oral hygiene is general index of health…
visit your dentist regularly…
 prevention is better than cure 

44. THANK YOU
Submitted by
Aghil Madathil
CRRI
JKKNDC