this ppt describes about problems with gingiva and periodontium

2. Gingival And
Periodontal Diseases
In Children
Dr. Prasannakumari
Dept of pedodontics

3. Introduction

4. • In maintenance of the tooth in the oral cavity, the health
of the periodontium is very important.
• Prevalence of gingivitis in children has been reported to
be as high as 99%.
• Gingivitis when occurs…..it is limited to marginal gingiva.
• Destructive forms of periodontal disease is lower in
young individuals than in adults.

5. Gingival Characteristics
• Colour: Pink (parfitt 1973) or
Red (magnusson 1981)
Colour varies according to
Degree of vascularity
Epithelial keratinisation
Pigmentation
Thickness of epithelium

6. Surface texture
Size
Contour
Shape
Consistency
Orange peel appearance

7. Size: the size of gingiva corresponds with sum of cellular & intercellular elements and their vascular
supply
Alteration is a common feature of gingival disease
The contour or shape varies considerably & depends on the shape of the teeth & alignment in the
arch, the location, & size of the area of interproximal contact, the dimension of lingual & facial gingival
embrasure
Labial version- more apical- accentuated
Lingual- thicker n rounder

8. Stippling is a form of adaptive specialization or reinforcement for function
Feature of healthy gingiva
Seen on attached gingiva n center of interdental gingiva
Prominent on facial surface
Varies with age: appears about 5 yrs, increases untill adulthood, disappears in old age
Shape: shape is governed by- contour of proximal tooth surfaces & location, shape of gingival embrasure
interdental bone- thin MD, the gingival embrasures & interdental gingiva are narrow MD
the height of interdental gingiva varies acc to location of proximal contact
So anterior – pyramidal shape
Posterior more flattened

9. CHILDREN ADULT
MARGINAL
GINGIVA
Thicker and rounder due to cervical
bulge and underlying constriction
Flaccid, retractable due to
immature connective tissue and
gingival fiber system and also due
to increased vascularisation
Thin & Knife edge
ATTACHED
GINGIVA
Flaccid, Less dense, red
and less stippled, greater width
Firm & Resilient
More stippled
INTERDENTAL
GINGIVA
saddle areas Pyramidal or “col” shape
GINGIVAL
SULCUS
1-2mm 2-3mm
ALVEOLAR
MUCOSA
Thin epithelium & absence of
keratin
Thick epithelium and more keratinized
Difference between Children and adult periodontium

10. • Interdental clefts
• Retrocuspid papilla
• Periodontal space is wider with few fibers
• Alveolar bone:
less calcified, more vascular
Few but thicker trabeculae
Larger marrow space
Prominent lamina dura
Flattened interdental crests

11. • Gingivitis is common than periodontitis
• Gingivitis is transient and acute compared to progressive
and chronic in adults
• more anabolic activity
• due to increased metabolism absence of bacteria
responsible for periodontal disease such as spirochetes
and b.melaninogenicus, altered composition ofplaque
and decreased leukocytic migratory rate due to low
levels of immunoglobluins specific for plaque bacteria
and decreased vascular inflammatory response

12. GINGIVAL DISEASES

13. Stages of gingivitis
Stage 1: INITIAL STAGE (subclinical gingivitis)
Stage 2: EARLY STAGE
Stage 3: ESTABLISHED STAGE
Stage 4: ADVANCED STAGE (phase of periodontol breakdown)

14. 1st manifestation: vascular changes- dilated capillaries, increased blood flow
Initial response of the gingiva is not apparent clinically
2nd stage develop after 1 week of plaque accumulation
Appears as early gingivitis
Signs of erythema
Bleeding on probing
2-3 weeks after plaque accumulation
Blood vessels-engorged and congested, venous return impaired-blood flow
sluggish- resulting in localized gingival anoxemia ( bluish hue on reddened
gingiva
This stage: moderately to severely inflamed gingiva
4th:: Extension of the lesion into alveolar bone

15. Simple gingivitis
Earliest sign
“Increased gingival crevicular fluid production rate
Bleeding from gingival sulcus on gentle probing”
• Color changes
• Surface texture
• Change in position- not seen
Management: oral prophylaxis, oral hygiene measures
“Gingivitis in children largely reversible”

16. Eruption gingivitis
• Temporary form of gingivitis
• Often associated with difficulty in eruption subsides after
emergence of tooth
• Commonly seen- 1st & 2nd permanent molar
• Treatment: proper oral hygiene measures

17. Pubertal gingivitis
Features: Enlarged interdental areas
Spontaneous bleeding from the gingiva
Management: oral prophylaxis
proper oral hygiene maintenance
Scorbutic gingivitis
Features: Limited to marginal tissue, papilla
Severe pain & spontaneous hemorrhage
Management: complete dental care, improved oral hygiene,
supplementation of vit c, water soluble vitamin

18. Gingivitis associated with
mouth breathing
Treatment: remove the cause of local obstruction
Pseudomouthbreathers: oral screen

19. Necrotizing ulcerative gingivitis
Also called as Ulcerative gingivitis
Acute necrotizing gingivitis
Vincent’s infection(stomatitis)
Fuso spirochetal disease
Trench mouth
Peak incidence- late teens, 20’s
Occasionally 6-12 years

20. Causative organism : spirochetes, fusiform bacteria
Local predisposing factors: erupting teeth, inadequate restorations,
calculus accumulations, occlusal trauma,
poor oral hygiene, preexisting gingivitis
Systemic predisposing factors: Nutritional deficiency
Debilitating disease
Primary diagnostic features Secondary diagnostic features
Interdental ulceration & necrosis
Pain
Bleeding
Elevated temperature with resultant
blunting & cratering of gingiva
Pseudomembrane
Fetid mouth odor
Bad taste

21. Treatment:
Local debridement
Subgingival curettage, use of mild oxygenating solutions
Antibiotic of choice- penicillin or erythromycin, metronidazole
Analgesics
Mild & moderate
stage
In severe cases
In very severe cases
Local lymphadenopathy , Slight elevation in
temperature
Gingival soreness, metallic taste, excessive
salivation, halitosis
high fever, increased pulse rate, leucocytosis,
loss of appetite, General lassitude
noma, fusospirocheatal meningitis&
peritonitis, pulmonary infections, toxemia,
fatal brain abscess
Symptoms:

22. Primary Herpetic Gingivostomatitis
• Caused by the herpes Simplex Virus (type 1)
• Mostly occurs in a child under 6years of age
• Course of the disease: 7-10 days

23. • Symptoms: Generalized Soreness of the oral cavity, Pain,
Cervical adenitis, high Fever, Generalized malaise
• Management: Bed rest
Antipyretics, analgesics
Application of mild topical anesthetic
Drink lot of oral fluid, soft diet
In severe case: antiviral medications
Isolation from siblings, peers- to prevent spread of infection

24. Necrotising ulcerative gingivities Primary herpetic gingivostomatitis
Interaction between host and bacteria
Necrotizing condition
Punched out gingival margin,
pseudomembrane
Interdental gingiva affected
Uncommon in children
no definite duration
Specific viral etiology
Diffuse erythema & vesicular eruption
Oval or Spherical ulcer
Diffuse involvement
Common in children
7-10 days

25. Gingival enlargements
I
II
III
IV
V
Inflammatory enlargements
Chronic , Acute
Drug induced enlargements
Enlargements associated with systemic diseases or condition
- Conditioned enlargements
(Pregnancy, Puberty, Vitamin c def, Plasma cell gingivitis,
Nonspecific conditioned)
- Systemic diseases
(Leukemia, Granulomatosis diseases)
Neoplastic enlargements
Benign, Malignent
False enlargements

26. Degree of gingival enlargements can be scored as
Grade 0: No signs
Grade I: Confined to interdental papilla
Grade II: Involves papillary and marginal gingiva
Grade III: Covers 3 quarters or more of the crown

27. Chronic inflammatory enlargements
• Most prevalent type
• Etiology: prolonged exposure to the dental plaque
• Clinical features:
limited to marginal & papillary gingiva
Gingiva- red or bluish red, soft , friable,
smooth shiny, surface, bleed easily
• Treatment: rigorous plaque control
oral prophylaxis

28. Acute inflammatory enlargements
Gingival abscess
• Localised, painful, rapidly expanding lesion that is usually of
sudden onset
• Etiology: bacteria carried deep into tissues
• c/f: Generally limited to the marginal gingiva or interdental
papilla
• Treatment: incision

29. Drug induced gingival enlargements
Anticonvulscents,
Immunosuppresents
Calcium channel blockers

30. Phenytoin induced gingival hyperplasia
It appears as early as 2-3 weeks after
initiation of phenytoin therapy & peaks at
18-24 months
Initial clinical appearance: painless
enlargement of interdental gingiva
Buccal, anterior more than lingual &
posteriors
Unless a secondary infection or
inflammation is present, the gingiva appears
pink & firm, doesn't bleed on probing
As there is continuous growth of interdental
gingiva, clefting become prominent in
midline of the tooth, clefting coalesce-
forming pseudopockets, covering the crown
structure

31. Enlargements occurs in 50% of the patients receiving the drug
Prevalence
- Younger age group
- Increasing dose
- Increasing serum phenytoin levels
- Decreasing degree of oral hygiene
Treatment: replacement of the drug
Oral prophylaxis
Use of chlorhexidine
specific surgical approach

32. Enlargement associated with
systemic disease
• Is a disease characterized by progressive overproduction of WBC,
which usually appear in circulating blood in immature form
• Occurs in acute leukemia
• Diffused or marginal,
• Localized or generalized
• Appear as diffused enlargement of the gingival mucosa Or discrete
tumor like interproximal masses
• Bluish red, shiny cyanotic surface
• Rounding & tenseness of the gingival margin covers crown
• gingival hemorrhage- common- due to ulceration of sulcus
epithelium, necrosis of underlying tissue

33. • Gingivitis, Gingival hyperplasia, Petechia, hemorrhage, Ulceration of the
mucosa
Management: BT ,CT & platelet count should be checked , hematologist
should be consulted before periodontal treatment
Scaling & curettage
Plaque control
Administer antibiotics

34. Periodontitis in children

35. Chronic Periodontitis
(Old Term-adult Onset Periodontitis)
• Defined as an infectious disease resulting in
inflammation within the supporting tissues of the
teeth, progressive attachment loss and bone loss

36. • Can occur in children & Adolescent
• Primary & permanent dentition –affected
• Symptoms: bleeding of gums, spacing, loose tooth, sensitivity,
food impaction
• Clinical features: plaque accumulation, gingival inflammation,
pocket formation, gingival bleeding
• Can be localized: <30%
Or generalized : >30%
Treatment: Oral hygiene instructions
Scaling root planing,
Correction of local contributory factors
Maintenance of oral hygiene

37. Aggressive Periodontitis
(Old Term: Early Onset Periodontitis)
• Localized aggressive periodontitis
(replaces localized juvenile periodontitis,
localized early onset periodontitis)
• Generalized aggressive periodontitis
(replaces generalized juvenile periodontitis,
generalized early onset periodontitis)
• Localized or generalized aggressive periodontitis occurring
prepubertally
(replaces prepubertal periodontitis)
Generally affect systemically healthy individuals less than 30yr old
Distinguished from chronic by age of onset

38. Localized Aggressive Periodontitis
• Etiology: hereditary
• Characterised by- localised 1st molar or incisor presentation
with interproximal attachment loss on atleast 2 teeth
• striking feature:
“Lack of clinical inflammation despite the presence of deep pd
pocket & advanced bone loss”
• Distolabial migration of maxillary incisors
• Mobility
• Deep, dull, radiating pain during mastication
• Root sensitivity

39. • Radiographic finding: vertical loss of alveolar bone around 1st
molars & incisors
“Arc shaped bone loss”
Loss of bone 3-4 times faster than chronic periodontitis
• Treatment: Subgingival irrigation
Scaling and root planing &
Systemic tetracycline therapy

40. Generalized aggressive
periodontitis
• Generalized interproximal attachment loss affecting atleast 3
teeth other than 1st molar & incisor
• Gingival condition: can be severely inflamed, or can be normal
• Treatment: Subgingival irrigation
Scaling and root planing &
Systemic tetracycline therapy

41. Prepubertal periodontitis
• Tends to occur in families
• Females> males
• It may began around 4years or before, may not be diagnosed
until 7-9 years
• Prevalence –less than 1%
• Clinical features: attachment loss, bone loss around primary
teeth
Defective peripheral blood leukocyte function, defects in
neutrophil or monocyte function

42. Treatment:
Curettage, antibiotic therapy, improved oral hygiene
Generalized Localized:
All primary teeth –affected, permanent
may or may not
Extremely acute gingival inflammation
Rapid destruction of the alveolar bone
Functional defect of peripheral blood
neutrophils & monocytes
Otitis media, upper respiratory infections
Refractory to antibiotics
Only few affected
Less inflammation
Destruction is not rapid
Same
Not frequent
Amenable to curettage, antibiotic

43. Periodontitis associated with
systemic diseases

44. Etiology: unknown
- Endocrinopathy
- Vit A deficiency
- Bacteriodes gingivalis & capnocytophaga
Papillon-lefevre syndrome
Treatment: Vitamin A metabolites

45. Hyperkeratosis- starts 1st & 4 yr
after birth
It is progressive becomes dry&
scaly, deep n painful fissures in
winter
Primary dent- normal in development &
age of eruption
As soon as last decidous tooth erupts:
swollen gingiva, migration, mobility of
teeth pockets, exfoliation
By 3-4 yrs. all teeth are lost.
after loss-inflammation regresses
Eruption of permanent- enhanced,
completed by 5 yrs.
The disease recycles13-14yr-exfoliated
Ectopic intracranial calcifications

46. Hypophospatasia
(rathbun syndrome)
• Rare genetic disorder manifested by bone pain with spontaneous
fractures, rickets like bone lesions during childhood which are
resistant to treatment with vitamin D, premature loss of the
deciduous tooth
• Etiology:
familial disorder- recessive autosomal
deficiency of the enzyme alkaline phosphatese in serum or tissues
excretion of phospho-ethanelomine in urine

47. Divided in 3 forms
1) infantile type (Birth & 6month of age)
2) Childhood type (6-14 month)
3) Adult type (During childhood)
Treatment:
Oral phosphate supplements
DISEASE IS
CHARACTERISED BY
abnormal mineralization of
bone & dental tissues
Manifested by premature
exfoliation of the primary
teeth(75% of pt) 1st clinical
sign
Only deciduous incisors, are
affected, sometime canine ,
permanent- normal

48. Cyclic neutropenia
Def: “It is a unusual form of agranulocytosis characterized
by periodic or cyclic diminution in circulating
polymorphonuclear neutrophilic leukocytes as a results of
bone marrow maturation arrest, accompanied by mild
clinical manifestations, which spontaneously regresses
only to recur subsequently in a rhythmic pattern.”

49. Disappearance occurs approx every 3 weeks, after 5-10 days
neutrophil begin to reappear
During neutropenic stage: periodontal destruction
Non neutropenic stage: oral health returns
Prognosis: are at risk
for fatal bacterial
infection during this
stage

50. Skin lesions,
ear infections
Mouth ulcerations,
Stomatitis
Papillary gingiva, marginal gingiva- enlarged edematous,
bleeds easily
Bone resorption progresses rapidly
Antibiotic therapy –ineffective

51. Chediak-higashi syndrome
• Rare Autosomal recessive immunodeficiency disorder
• Disease affects the production of organelles found in almost
every cell
• Affects melonocytes, platelet, phagocytes
• Causes partial albinism, mild bleeding disorders, recurrent
bacterial infections, photophobia, nystagmus, peripheral
neuropathy
• Oral manifestation: severe gingivitis, periodontitis, ulceration
of mucosa, tongue & hard palate

52. • Leukocyte adhesion defect(LAD)
Autosomal recessive defect
“ Prepubertal generalized aggressive periodontitis”
• Acute leukemia:
gingiva- hyperplastic, edematous, bluish red, petechie,
mucosal ulcerations
• Langerhans cell histiocytosis
Bone lesion: floating teeth, gingival swelling

53. Insulin dependent diabetes(type I)
- Increased incidence of gingivitis
- Earlier onset of periodontitis
- Alv bone resorption
- Xerostomia
- Recurrent gingival abscesses
- Increased susceptibility to infections, reduced wound healing
- Both premature & delayed eruption of permanent teeth is observed
Management:
- Normal diet before dental appointment
- If the dental procedure is anticipated to be stressful- consult the physician for
adjustment in the insulin dosage
- Prophylactic antibiotic- recommended before procedure

54. Necrotizing ulcerative periodontitis
“ Cases of NUP are being described in immunocompromised patients(HIV)”
Diagnosis of NUP to be a marker for diagnosis of AIDS
Distinctive feature: periodontal attachment & bone loss
Other features: Deep interdental osseous craters
Advanced lesion: severe bone loss, tooth mobility,
ultimately tooth loss
Oral malodour, fever, malaise or lymphadenopathy
Etiology: fusiform-spirochete bacterial flora,
Various predisposing factors,
immunocompromised state
Stress, malnutrition