DR RACHAEL GUPTA M A RANGOONWALA DENTAL COLLEGE PUNE

1. 1
PERIODONTAL
DISEASES in children
By- DR.RACHAEL GUPTA

2. Contents
• Introduction
• Anatomical consideration in children
• Periodontal diseases: PERIODONTITIS(definition)
• Age changes in PDL
• Why periodontal diseases are less in children?
• Periodontal examination of children
• Epidemiology of periodontal diseases
• Classification
• Early onset periodontitis
• Prepubertal periodontitis
• Localized early onset periodontitis
• Generalized early onset periodontitis
• Systemic diseases and conditions with associated periodontal problems

3. o Consists of investing and supporting tissues of the tooth.
INTRODUCTION
Periodontium
Gingiva
Attachment
Apparatus
Periodontal
Ligament
Cementum
Alveolar
Bone

4. • Alternative names – desmodont,
gomphosis, pericementum, dental
periosteum, alveolodental ligament,
periodontal membrane
• Average width – 0.2 mm
PERIODONTAL LIGAMENT

5. CEMENTUM
Calcified, avascular
mesenchymal tissue that
forms the outer
covering of the anatomic root.
OR
Hard, avascular connective
tissue that covers the roots of
the teeth.

6. ALVEOLAR PROCESS
• Portion of maxilla and mandible that
forms and supports tooth socket.
• Forms when tooth erupts.
• Disappears gradually after tooth is
lost.
• Tooth dependant bony structures .

7. Features of differentiation Permanent dentition Primary dentition
PERIODONTAL
LIGAMENT
Thickness 0.2 mm Thicker than perm. teeth
CEMENTUM No significant clinical
changes
ALVEOLAR BONE
Lamina dura Thinner & denser Wider & less dense
Interdental crest Resembles hill top Flat
Bone density Denser, calcification higher Less calcified, more vascular
Bone marrow volume Lesser Large

8. Anatomical consideration in children
PERIODONTAL LIGAMENT
• PDL space - wider,
• PDL - fewer and less dense fibers per unit area.
• less fibrous and more vascular
CEMENTUM
• thinner and less dense.
• Children show a tendency for hyperplasia of cementum apical
to the epithelial attachment.

9. ALVEOLAR BONE
• the lamina dura is thinner , fewer trabeculae and large marrow
spaces.
• There is greater amount of blood and lymph supply.
• The crest of the bone appears flatter.

10. PERIODONTAL DISEASES
PERIODONTITIS:
Inflammatory disease of the gingiva
and deeper tissues of the
periodontium, characterized by
pocket formation and destruction of
supporting alveolar bone.
Dentistry For The Child & Adolescent, MCDONALD, 9th EDITION.

11. Age changes in PDL
• Fiber and cellular contents decreases with age.
• Principles fibres get thickened and become irregular and wavy.
• Decreased cell density and reduction in organic matrix production
with advancing age.
• Degenerative hyaline changes takes place.
Garg et al- Aging and periodontium
11

12. Ive et al (1980) also noted
the width of the socket and the width of cementum increased
with age;
they suggested that as the socket remodels and increses in size
with age , cementum is deposited at a relatively greater rate
than the bone causing decrease in the pdl space.

13. Why periodontal diseases are less in
children?
• The zone lying beneath the
interproximal contact area and
between the dental papillae is known
as the interdental col.
13

14. In the primary dentition interdental spacing is common, instead of col interdental
saddle areas are present resulting in a well-keratinized surface.
This feature may contribute to the lower prevalence of periodontal lesions ,
the saddle areas are less vulnerable to the development and progression of the
inflammatory process
(Ruben et al., 1971).

15. • Robinson (1951) proposed that the strong periosteal
activity found in children permits repair concurrent
or following disease and therefore offers a resistance
to development of periodontitis.
15

16. Periodontal examination of children:
• The gingival tissues should be examined for redness,
edema, bleeding, or enlargement.
• Oral hygiene may be assessed via a plaque index.
• Use of a disclosing agent provides an excellent oral
hygiene instruction tool
• Calculus is not as common in young patients as it is
in adults, but it is found in about 10% of children
• Patients should always be checked for calculus at
periodic examination visits, and deposits should be
removed.
16

17. EXAMINATION
• A simplified screening
system for the under-18s
as described by Clerehugh
and colleagues is quick
and easy to use in
practice. It involves
assessing index teeth
(UR6, UR1, UL6, LL6, LL1
and LR6) using a WHO 621
probe with a 0.5 mm ball
end and black band at 3.5
to 5.5 mm using BPE
codes 0 to 2 in 7- to 11-
year-olds and the full
range of codes 0, 1, 2, 3, 4
in 12- to 17 year-olds .
(V. Clerehugh, Periodontal diseases in children and
adolescents-BRITISH DENTAL JOURNAL VOLUME 204
NO. 8 APR 26 2008.)

18. • Although periodontal probing is the most reliable
way( Armitage 1995) some children might not
tolerate the slight discomfort that is involved.
• In such cases….radiographs and visual
examination.(Bimstein et al 1988, Sjodin et al 1993)
• In children …mixed dentition.. Several erupting
teeth.. probing depths greater than 3mm may
indicate “pseudopocketing” rather than true loss of
attachment.

19. • When radiographs are available, bone levels should be examined.
• Normal crestal height should be within 1 to 2 mm of the cemento-
enamel junction.

20. Epidemiology of periodontal diseases
• Prevalence :
Children (5-11yrs)  1-9%
Adolescents (12-15yrs)  1-46%
(Delaney 1986, Wei et al 1986,Papapanou 1996)
In Indian population – a study conducted in Lucknow in 3 schools-
Overall periodontitis was 16.03%(8 to 17yrs)
In Manglore - The prevalence of AP was found to be 0.36% and that of
CP was found to be 1.5 %. (J Indian Soc Periodontol. 2013 Nov-Dec)
Mathura city- 0.54 ± 0.88%(12yrs old children)

21. Loss of Periodontal support in Deciduous Dentition
• Bimstein et al. (1996)
Prevalence  26.8% Attachment loss
4.7% Absence of lamina dura
in children aged 6-9yrs
• Carranza et al. (1998)
Prevalence  7.8% in children aged 3-10yrs
Methods used :
Clinical Attachment Loss (CAL) –
Distance b/w CEJ & bottom of gingiva
Radiographic bone loss –
Complete absence of lamina dura
(JIMSON ET AL)

22. The Periodontal Disease Classification System of the AAP — An Update;
December 2000.
Classification

23. However, the 1989 classification had its
shortcomings including:
• lack of a category for strictly gingival
diseases;
• difficulty in fitting certain patients into
any of the existing categories;
• similarity of microbiological and host
response in dieases;
• an emphasis on age of onset that
became a problem as patients aged
into a new category; and some unclear
classification criteria

24. A new
periodontal
disease
classification
system was
recommended
by the 1999
International
Workshop for a
Classification of
Periodontal
Disease and
Conditions

25. EARLY ONSET PERIODONTITIS
• Albandar et al proposed the term early onset periodontitis
• Termed as aggressive periodontitis by AAP 1999
• EOP is used as a generic term to describe a heterogeneous
group of periodontal diseases occurring in young individuals
who are otherwise healthy
• EOP can be viewed as three categories of periodontitis
1. Prepubertal form
2. Localized form
3. Generalized form
25

26. Prepubertal periodontitis
• Page et al.first described prepubertal periodontitis, an extremely
rare category of periodontitis, as a distinct clinical entity.
• Onset - during or soon after the eruption of the deciduous teeth
• Both familial clustering of periodontitis and higher incidence in
females is documented
• Prepubertal periodontitis of the primary dentition can occur in a
localized form but usually is seen in the generalized form
26
Periodontology 2000, Vol. 26, 2001, 7–15

27. • CAUSES:
1. Abnormalities in host defence( eg:
leucocyte chemotaxis)
2. Family history of periodontitis have been
associated with LPP in children
3.Leukocyte defects found in PMN cells or
monocytic cells but not both.

28. Localized prepubertal periodontitis :
localized attachment loss and alveolar bone loss in the primary dentition
in an otherwise healthy child
Clinical features :
• affects some but not all of the primary teeth more often the molars
• Plaque deposits are moderate
• Little inflammation of gingiva
• Bleeding upon probing on affected sites
• No association with systemic diseases
• Destruction is not as rapid as generalized form by condition can respond
to T/T
• Bone loss is usually seen on radiographs around the primary molars
and/or incisors
• As the disease progresses, the child's periodontium shows signs of
gingival inflammation with gingival clefts and localized ulceration of
the gingival margin
Periodontology 2000, Vol. 26, 2001, 7–15

29. Generalized prepubertal periodontitis
• affects all the deciduous teeth and
sometimes also involves the
permanent dentition.
• acute inflammation of the gingival
tissues
• rapid destruction of the
periodontium, often leading to
premature exfoliation of the teeth.
• Pronounced recession and cleft
formation are also sometimes
present.
• The periodontitis may be refractory
to therapy.
Clinical features:

30. Individuals may suffer from recurrent
upper respiratory tract and skin
infections.
It has been suggested that this form of
prepubertal periodontitis is only found
associated with leukocyte adhesion
deficiency syndrome
However, generalized prepubertal
periodontitis has also been reported in
otherwise healthy children
Periodontology 2000, Vol. 26, 2001, 7–15

31. Testing may reveal:
• High prevalence of leukocyte adherence abnormalities
• Impaired host response against infection
Bacterial involvement:
1. Actinobaciilus actinomycetemcomitants
2. Porphyromonas gingivalis
3. Prevotella intermedia
4. Capnocytophaga sputigen
5. Fusobacterium nucleatum
31

32. • Treatment of LPP or GPP depends on early diagnosis
1. Dental curettage
2. Root planning
3.Oral hygiene instruction
4.Restoration of decayed teeth
5.Removal of the primary teeth that have lost bony
support and more frequent recalls
6.Use of antimicrobial rinses
7.Therapy with broad spectrum antibiotics are effective
in elimination the periodontal pathogens

33. • Treatment of GPP is less successful overall and
sometimes requires extraction of all primary
teeth
Delaney reported that children with LPP and
GPP may experience severe periodontitis of
permanent teeth

34. LOCALIZED EARLY ONSET
NTITIS
• Earlier known as localized juvenile periodontitis.
• Occurs: in healthy children and adolescents without clinical evidence of
systemic diseases
• CAUSES
1. Microbial species: Aa or Aa in combination with bacteroids
2. Neutrophil defects
3. Abnormalities in Peripheral blood neutrophil (PMN leukocyte chemotaxis )
Page et al
4. Bacterial activity
5. Hereditary basis for LJP( Page et al)

35. According to Hart et al.
diagnosis of localized early-onset periodontitis
is based on
• attachment loss of > or equal 4 mm on at least two permanent first molars
and incisors (one of which must be a first permanent molar)
• Not more than two other permanent teeth, which are not first permanent
molars or incisors, should be affected
• Bone loss around primary teeth can be early finding in LAP
Periodontology 2000, Vol. 26, 2001, 7–15

36. • C/F:
1. Patients have little or no tissue inflammation
2. Very little supra-gingival dental plaque or calculus
3. Progression of bone loss is there to four times faster than in adult periodontitis.
R/F:
• Bilateral angular bone loss around molars
• Characterized by the rapid severe loss of alveolar bone around more than one
permanent tooth, usually the first molar and incisor
• Retrospective data obtained from LJP patient suggest that bone loss around the
primary teeth can be an early finding in the disease
• Prevalence : of LJP range from 0.1%-1.5% with a bilaterally symmetric pattern of
bone loss in a geographically diverse adolescent population
• Prevalence in black population is greater at 2.5%
Mcdonald s,10th edition.

37. Generalized early onset
periodontitis
• Occurs at or around puberty in older juvenile and young adults
• CAUSES: microorganisms associated are porphyromonas gingivalis
• C/F:
often affects the entire periodontium of the dentition.
distribution and rapid rate of alveolar bone destruction
marked periodontal inflammation
have heavy accumulators of plaque and calculus.
Mcdonald s, 9th edition.

38. • The past medical history of the child often reveals a history
of recurrent infections(eg, otitis media,skin infections,upper
respiratory tract infections)
• Neutrophils in GAP patients have supressed chemotaxis
• Loe and brown –
• 0.13% prevalence of GAP amonf adolescents in US
• The localized and generalized form of EOP are distinctly
different radiographically and clinically
Mcdonald s, 9th edition.

39. Treatment of aggressive periodontitis
• Successful treatment of EOP depends on early diagnosis use of
antibiotics against the infecting micro organisms and provision of
an infection free environment for healing
• EOP both localized and generalized types includes surgery and
use of tetracyclines (Lindhe 1982,Christersson and Zambon
1993)
Mcdonald s, 9th edition

40. In pts of LAP,
Aa organisms penetrate into crevicular epithelium
T/T with antibiotic alone such as 2 week course of doxycycline reduce Aa
organisms
Surgical removal of infected crevicular epithelium and debridement of root surface
during surgery while the patient is on a 14 day course of doxycycline hyclate (1gm
per day)(Mandell and Sockaransky 1988,Saxen et al 1990).
Microdentex manufacturers the DMDx(Microdentex, FORT MYERS, Florida) test, a
DNA test kit for establisting the risk of aggressive periodontits and confirms
whether the child has responded favorably to the use of antimicrobial therapy
Retesting after 4-6 weeks after the completion of antibiotic therapy determines
the pts response to t/t
Mcdonald s, 9th edition

41. • Rams and collagues described keyes technique for treating LAP
Scaling and root planning of all teeth , with irrigation to probing
depth of saturated inorganic salt solutions and 1% chloramine-
T.((sodium para-toluene sulfonchloramide)
In addition recommended administration of systemic tetracycline
(1g per day) for 14 days
This dose appropriate for pts 12 yrs of age and older
Home T/T
Daily application of paste of sodium bicarbonate and 3% hydrogen
peroxide and inorganic salt irrigation
Mcdonald s, 9th edition

42. • T/T of GAP
- often less predictable
- alternative antibiotics directed to specific pathogenic flora
require
- Multidisplinary approach combines clinical labroartory
evaluation with conventional periodontal therapeutic
methods for diagnosis and t/t of GAP
Mcdonald s, 9th edition

43. Periodontitis as manifestation of
systemic disease

44. Hypophosphatasia
• Rare genetic disease manifested
• Autosomal inherited trait
• Inborn error in metabolism
• Insufficient level of alkaline phosphatase enzyme
• Increase in urinary exretion of phospoethanolamine
• Defective bone /tooth mineralization
44

45. • Clinical features:
• The disease occurs in severe and mild forms, and at least three types are
recognized.
• infantile type first appears between birth and 6 months of age.
childhood type appears between the ages of 6 and 14 months,
adult type manifests during early adult life and radiographically osseous
radiolucencies are seen.
• R/F : shell appearance due to the widening of the pulp chanber and root canal
• Skeletal radiographs show “spotty,” “streaky,” or irregular ossifications in the
metaphyses of the long bones
45

46. The disease is characterized
abnormal mineralization of bone and dental tissues and is usually manifested by
premature exfoliation of the primary teeth.
In almost all cases of hypophosphatasia the deciduous incisors and sometimes the
canines are affected and the permanent teeth are usually normal.

47. D/D- localized juvenile periododntits
Diagnosis:
Low levels of serum,liver ,kidney, and bone alkaline phosphatase and elevated
levels of phosphoethanolamine in serum and urine.
Treatment:
Oral phosphate supplements have been attempted with a limited success and
intravenous infusions of plasma no clinical benefits
47

48. Leukocyte adhesion deficiency
syndrome
• A recently defined immunological disease, leukocyte
adhesion deficiency (LAD), occurs when three surface
glycoproteins are absent or defective on leukocytes (PMN),
leaving affected patients susceptible to bacterial infections
(Crowley et al. 1980; Arnaout et al. 1982; Dana et al.
1984).

49. • Abnormal leukocyte function and decreased cellular adhesion.
• Early onset prepubertal periodontitis seen
• Severe periodontal disease
• Extreme inflammation & proliferation of gingival tissues
• Rapid destruction of bone immediately after eruption of deciduous
teeth.
• All primary teeth affected

50. One reported patient had all primary teeth extracted by age
three years because of periodontitis
The same patient lost several permanent teeth by age 12 years
as a result of 50-90% alveolar bone loss
Gingival biopsies obtained when teeth were extracted
demonstrated only a mononuclear infiltrate in the tissue
(Waldrop et al. 1987)
Additional reported oral findings in patients with LAD include
stomatitis, ulcerations of mucous membranes, and facial cellulitis
(Anderson and Springer 1987)

51. Papillon- lefevre syndrome
• The syndrome is rare and the cause is unknown
• Familial predisposition to the disorder is noted ,
autosomal recessive mode of inheritance has been
identified
• Causative gene for the syndrome by linking it to
chromosome band 11q14-q 21
• No gender and racial predominance
51

52. C/F:
the primary teeth erupted at the normal time
However as early as 2 years of age - painful
gingival tissue.
There is a tendency towards gingival bleeding
when the teeth are brushed
Hyperkeratosis of palms and soles present
The first evidence - erythema and scaliness noted
initially at 8 months of age
Repeated lab test including CBC,urinalysis, and
microserum calcium and phosphorus
determinations – normal results

53. • At 2 1/2 years of age all the
primary teeth - looseness and
severe horizontal bone
resorption
• Gingival inflammation
• Presence of infected
periodontal pocket, all
primary teeth removed by 3
yrs of age
53

54. Histogical examination:
Premature resorption pattern with normal pulp tissue
Cementum was normal and covered root structures
Accumulation of basophilic plaque , made of mass of filamentous
organisms
According to Tinamoff et al bacterial species asso. Are
aggregatibacter actinomycetemcomitans, fusobacterium nucleatum,
capnocytophaga. isolated

55. Treatment
• A combined approach including plaque control,
administration of chlorhexidine in combination with a
systemic antibiotic therapy for the eradication of known
periodontal pathogens in conjunction with retinoids
seems to be most promising as long as the precise
nature of the underlying genetic defect is still not
known
• Complete dentures were constructed 3 months after
removal of primary teeth
denture base were adjusted to allow for emergence of
teeth

56. Cyclic neutropenia
• The cyclic variety appears to be the type most frequently encountered in the
dental literature.
• The disappearance of neutrophils occurs periodically, approximately every 3
weeks. After 5 to 8 days, the neutrophils begin to reappear.
• It is inherited as an autosomal recessive disorder.
Clinical features:
• These patients have periodic symptoms including skin lesions and ear
infections.
• Mucous membrane ulcerations, severe stomatitis are reported

57. • Gingival enlargement,edematous and erythematous
and bleed easily on a gentle provocation.
• There is an extreme inflammation with proliferation
of the marginal gingiva accompanied by a cleft
formation, recession;
• antibiotics are ineffective and bone resorption
progresses rapidly to the apex of the teeth.
• During the neutropenic stage, periodontal disease
and destruction occurs and during the non-
neutropenic stage oral health returns.
• Overall, the destruction exceeds repair and alveolar
bone loss contributes to an early exfoliation of
teeth.
57

58. Chediak higashi syndrome
• Linked with severe periodontitis
• Rare autosomal recessive immunodeficiency disorder
• Characterized by large lysosomal granules in
granulocytes, oculocutaneous infections and
intermittent febrile episodes
• Dental aspects:
early-onset periodontitis, ulcerative lesions of the gingiva,
a haemorrhagic inflammatory response of the marginal
gingiva,
tooth exfoliation

59. • t/t
Functional defects are corrected by ascorbic acid
Other t/t consisted of management regimens
Etoposide-corticosteroids
Intrathecal methotrexate
High dose of intravenous gobulin

60. Leukemia:
• Leukemia is a disease characterized by the progressive
overproduction of white blood cells, which usually
appear in the circulating blood in an immature form
Oral manifestations:
• Oral lesions occur in both acute and chronic forms of
all types of leukemia; myeloid, lymphoid and
monocytic.
• These manifestations are far more common, however,
in the acute stage of the disease and are most
common in monocytic leukemia
60

61. • These primary clinical manifestations of the
disease may consist of
gingivitis, gingival hyperplasia, hemorrhage,
ulceration of the mucosa.
• True leukemic enlargement occurs commonly in
acute leukemia ,It seldom occurs in chronic
leukemia.
61
• Leukemic enlargement may be
• diffused or marginal,
• localized or generalized.
It may appear as a diffused
enlargement of the gingival
mucosa, an oversized extension of
the marginal gingiva, or a discrete
tumor like interproximal mass.

62. The gingiva - bluish red and has a
shiny surface with a rounding of
the gingival margin, then it
increases in size, most often in the
interdental papilla and covering
partially the crowns of the teeth.
Gingival hemorrhage, which
commonly occurs is due to
ulceration of the sulcus epithelium
and necrosis of underlying tissue.

63. Treatment:
• The most common form of leukemia in children, acute lymphocytic leukemia,
a prolonged remission and probable cure rate approaching 50%.
• Bleeding and clotting times and platelet count of the patient should be
checked and the hematologist consulted before periodontal treatment is
instituted.
• The enlargement -scaling and curettage carried out in stages under topical
anesthesia.
• The initial treatment consists of gently removing all loose accumulations with
cotton pellets, superficial scaling, and instructing the patient in oral hygiene for
plaque control.
• Antibiotics are administered systemically, the evening before and for 48 hours
after each treatment to reduce the risk of infection.
63

64. Diabetes:
• An increased risk and earlier onset of periodontitis occur in
both insulin dependent (IDDM) and non-insulin dependent
diabetes mellitus (NIDDM) , probably because of impaired
immune function.
• As many as 10% to 15% of teenagers with IDDM have
significant periodontal disease.
• Poor metabolic control increases the risk of periodontitis, and
untreated periodontitis in turn worsens metabolic control of
diabetes.
• Effective preventive regimens and early diagnosis and
treatment of periodontitis are important for the overall health
of patients with diabetes.
• Periodontitis in IDDM (after 12yrs) more common
• Prevalence 9.8% in 13-18yr old
• More bone loss around 1st molars & incisors
64

65. Down’s syndrome:
• Down syndrome – autosomal chromosomal anomaly associated with
trisomy of chromosome 21
• High prevalence of chronic inflammatory periodontal disease in children
described by Cohen et al. (1961) and Johnson and Young (1963), but it
was first described by Brousseau (1928).

66. • Nature of condition:
Mental handicap
T-cell immunodeficiency and inappropriate enzyme
regulation
Functional defects in neutrophils and monocytes
Abnormal capillary morphology
Hyperinnervation of gingivae
These patients harbor relatively high levels of subgingival black –pigmented
anaerobic rods, spirochetes and actinobacillus actinono.

67. Plaque levels are high in these
patients
Severe recession in the mandibular
anterior region
a high frenum attachment is also
common in down syndrome.
Various authors found increased prevalence of periodontitis in
Down’s syndrome (Barnett et al., 1986; Loe and Holm-Pederson,
1900; Agholme et al., 1999).

68. • DEFINITION :
Acute suppurative inflammation of deeper periodontal
tissues caused by an infection of pyogenic bacteria
• C/F :
Overlying gingiva / mucosa distended & edematous
• shiny with red to reddish-blue hue
• Tissues painful to palpation, purulent exudate
expressed
• Tooth may extrude & exhibit increased mobility
• Tooth sensitive to occlusion or mastication /
percussion
• Regional lymphadenopathy, fever
Periodontal Abscess

69. • TREATMENT :
• Objective: drainage and debridement to relieve pain
• If very poor prognosis …then extraction followed by debridement of
the socket.
Root planing & drainage through gingival sulcus
Incision & drainage  extensive lesions
R/F :
Distinct radiolucency along the lateral aspect of the
root

70. Necrotizing Ulcerative Periodontitis
• C/F :
Two most significant findings used in the diagnosis
Of NPD –
Presence of interproximal necrosis and ulceration
Rapid onset of gingival pain
- pt is often febrile
- high levels of spirochetes and P. intermedia
R/F :
Loss of interproximal bone
• PATHOGENESIS :
Neutrophilic inflammatory infiltrate extends deeper
Rapid destruction of attachment apparatus
Exposure of alveolar bone
Tooth mobility & eventual exfoliation

71. Factors that predispose children to NPD include
viral infections (including HIV),
malnutrition,
emotional stress,
lack of sleep,
a variety of systemic diseases
T/T :
Mechanical debridement
Oral hygiene instruction and careful follow up
Debridement with ultrasonics has been shown to be particularly effective and
results in a rapid decrease in symptoms.
If the patient is febrile, antibiotics may be an important adjunct to therapy.
Metronidazole and penicillin - drugs of choice.
Periodontal Diseases of Children and
Adolescents AAP

72. REFERENCES:
 Dentistry For The Child & Adolescent, MCDONALD, 10th EDITION.
The American Academy Of Pediatric Dentistry (Aapd) Guidelines 2013.
DCN-2000 Gingival and periodontal diseases in children.
• Periodontal And Gingival Health And Diseases In Children, Adolescents, And
Young Adults. 1st Ed. By Enrique Bimsten.
• The Periodontal Disease Classification System of the AAP — An Update;
December 2000..
Newman, Takei, Klokkevold, Carranza. Carranza’s clinical periodontology, 11th
edition, India, Elsevier, 2012.
Shafer’s textbook of oral pathology. 5th edition.
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