periodontal diseases

1. CLASSIFICATION OF
PERIODONTAL DISEASES

2. Contents
 Introduction
 History
 Dominant Paradigms in the historical
development of classification systems
 Classification systems
 Conclusion
 References

3. Introduction
 Systematic arrangement into classes or
groups based on perceived common
characteristics.
 A means of giving order to a group of
disconnected facts.

4. Need for classification
 Provides a framework for scientifically studying
 Etiology
 Pathogenesis
 Treatment
 To assess the prognosis, outcome and
determine the treatment plan.

5. Advancing age and leads
to progressive loosening
and loss of teeth.
Very aggressive type
that occurs in younger patient
History
 Giralamo Cardono
 Fauchard (1723) – ‘Scurvy’ of the gums
 Early 19th century – Riggs Disease (John W Riggs
1811-1885)
1st to differentiate
periodontal diseases

6.  Gottlieb, 1920s
 Schmutz-Pyorrhoe
 Alveolar atrophy or Diffuse atrophy
 Paradental-Pyorrhoe
 Occlusal trauma
 Alveolar atrophy or Diffuse atrophy :
Accumulation of deposits, inflammation,
shallow pockets, and resorption of the alveolar crest.
Non inflammatory disease - loosening of teeth,
elongation,and wandering of teeth ,no dental deposit
Pockets are formed only in later stages

7.  Paradental-Pyorrhoe:
 Occlusal trauma :
Irregularly distributed pockets - shallow to
extremely deep. May start as Schmutz-Pyorrhoe
or as diffuse atrophy.
Physical overload which results in resorption
of the alveolar bone and loosening of teeth.

8.  McCall & Box : Periodontitis - those
inflammatory diseases in which all three
components of the periodontium
Periodontitis
 Simplex periodontitis
 Complex periodontitis

9. Dominant paradigms in the historical
development of classification systems
1870–1920 The clinical features of the
diseases
1920–1970 The concepts of classical
pathology
1970–present Infectious etiology of the diseases

10. Clinical characteristics paradigm (1870-1920)
 Local factors Black (1894), WD Miller (1890), Patterson (1885),
Riggs(1882)
 Systemic disturbances Peirce (1892), GA Mills (1881), LL Dunbar
(1894)
 Both local and systemic factors WD Miller (1890), Patterson
(1885)

12. C.G. Davis (1879)
 Gingival recession with minimal or no inflammation.
 Periodontal destruction secondary to ‘lime deposits’.
Mechanical pressure → alveolar bone resorption
because of lack of nutrition.
 Riggs’ Disease
‘... loss of alveolus without loss of gum.’ The
perceived problem was a ‘necrosed alveolus’ or
death of the periodontal membrane.

13. G.V. Black (1886)
 Constitutional gingivitis
 A painful form of gingivitis
 Simple gingivitis
 Calcic inflammation of the peridental membrane
 Phagedenic pericementitis (phagedenic =
spreading ulcer or necrosis)
‘Phagedenic pericementitis’ ‘Chronic
suppurative pericementitis’

14. Drawbacks/ Limitations:
 Little or no scientific evidence was used
 No accepted terminology or classification
system was adopted
Pyorrhea
alveolaris
Phagedenic
pericementitis
Calcic
inflammation of
the peridental
membrane
Riggs’ disease
Chronic
suppurative
pericementitis

15. Classical pathology paradigm (1920-1970)
 Gottlieb and Orban
 All disease categories labeled as ‘dystrophic’,
‘atrophic’, or ‘degenerative.
Inflammatory
Non- inflammatory
(degenerative/dystrophi
c)

17. INFLAMMATION
1. Gingivitis (little or no pocket formation; can include ulcerative
form – Vincent’s)
A. Local (calculus, food impaction, irritating restorations, drug
action etc)
B. Systemic (Pregnancy, Diabetes, Other Endocrine
Dysfunctions, Tuberculosis, Syphilis, Nutritional
Disturbances, Drug Action, Allergy, Hereditary, Idiopathic.
Etc)
2. Periodontitis
A. Simplex– bone loss, pockets, abscesses can form, cases
have calculus
B. Complex – etiologic factors similar to periodontitis, cases
have little, if any calculus.
ORBAN 1942

18. DEGENERATION
1. Periodontosis (attacks young girls and older men; often caries
immunity)
A. Systemic disturbances (Diabetes, Endocrine dysfunctions, Blood
dyscrasias, Nutritional disturbance, Nervous disorders, infectious
diseases)
B. Hereditary
C. Idiopathic
2. Atrophy
Periodontal atrophy (Recession. No inflammation no pockets;
osteoporosis)
(Local trauma, Presenile, Senile, Disuse, Following inflammation,
Idiopathic)
3. Hypertrophy
Gingival hypertrophy (Chronic irritation, Drug action, Idiopathic)
4. Traumatism (Periodontal traumatism, Occlusal trauma)

19. World workshop
in Periodontics
(1966)
• Periodontosis as a distinct disease
entity ???????
World workshop
in Periodontics
(1977)
• No scientific basis for retaining the concept
: non-inflammatory or degenerative forms
of destructive periodontal disease.
Periodontosis -
Infection
Juvenile periodontitis

20. Infection/ host response Paradigm (1970-
present)
 Robert Koch (1876) - The germ theory of
disease
 W.D. Miller - Early proponent of the infectious
nature of periodontal diseases
 Pyorrhea alveolaris:
 Predisposing circumstances

21.  Systemic conditions
 Reluctance to accept
 Degenerative nature of periodontal diseases
(i.e. domination of the ‘Classical Pathology’
paradigm).
 Microbiological studies

22.  Harald Löe (1965-1968) - classical
‘experimental gingivitis’
Infection/Host Response
Paradigm - Dominant
paradigm

24.  GINGIVITIS
Chronic Marginal Gingivitis
Acute Necrotizing Ulcerative Gingivitis (ANUG)
 PERIODONTITIS
Juvenile Periodontitis
Rapidly Progressive Periodontitis
Adult Type Periodontitis
PAGE AND SHROEDER 1982

25. Suzuki, 1988
 Modification of Page & Schroeder 1982
 3 plausible hypothesis for the pathogenesis of
the disease:
 Direct tissue destruction by bacteria &
metabolic products
 Immune hyper-responsiveness
 Immune deficiencies involving neutrophil
function (chemotaxis and phagocytosis)

26. Adult Periodontitis > 35 yrs
Rapidly Progressing Periodontitis
Type A 14 - 26 yrs
Type B >26 yrs
Post juvenile Periodontitis 26 – 35
yrs
Juvenile Periodontitis 12 – 26 yrs
Prepubertal Periodontitis < 14 yrs
SUZUKI
1988

27. Modifications :
 Subdivisions to rapidly progressive periodontitis
 Post- juvenile periodontitis
Advantages :
 Short and Easy
Shortcomings :
 Does not include all criteria and conditions like
gingival conditions

28. I. Adult Periodontitis
II. Early Onset Periodontitis
A. Prepubertal Periodontitis
1. Generalised
2. Localised
B. Juvenile Periodontitis
1. Generalised
2. Localised
C. Rapidly Progressive Periodontitis
III. Periodontitis Associated With Systemic Diseases
Downs syndrome, Diabetes, Papillon-Lefevre syndrome, HIV, others
IV. Necrotising Ulcerative Periodontitis
V. Refractory Periodontitis
WORLD WORKSHOP IN CLINICAL PERIODONTITIS,
1989

29. Merits:
 Inclusion of ‘Periodontitis Associated with
Systemic Disease’
 Inclusion of ‘Refractory periodontitis’

30. Critical evaluation
 Depended heavily on the age of the affected
patients Baab DA(1986), Page RC (1983) and the rates of
progression Page RC (1983).
 The dividing line between adult and early onset
categories -35 years.
 ‘Rapidly Progressive’ and ‘pre-pubertal
periodontitis’ - not a single entity
 Periodontitis

31.  Overlap exists among different diagnostic
categories and cases did not clearly fit into any
single category’
 Considerable ‘heterogeneity’ existed within the
Refractory Periodontitis
 KS Kornman (1996)
 Loe (1993)
 Choi J-I (1990), Lee et al(1995),
Magnusson(1991)

32. I. Periodontitis In Adults
II. Periodontitis In Juveniles
Localized Form
Generalized Form
III. Periodontitis With Systemic Involvement
Primary Neutrophil Involvement Disorders
Secondary/Associated Neutrophil Impairment
Other Systemic Diseases
IV. Miscellaneous Conditions
GENCO,
1990

33. Shortcomings:
 Onset, duration of diseases not considered
 Gingival diseases not considered

34. I. Gingivitis
Gingivitis, Plaque Bacterial
Non - Aggravated
Systemically Aggravated
Related To Sex Hormones
Related To Drugs
Related To Systemic Diseases
Necrotising Ulcerative Gingivitis
Systemic Determinants Unknown
Related To HIV
Gingivitis, Non-Plaque
Associated With Skin Disease
Allergic
Infectious
RANNEY, 1993

35. II. Periodontitis
Adult Periodontitis
Non-Aggravated
Systemically Aggravated
Neutropenia, Leukemias, Lazy Leukocyte Syndrome, AIDS, Diabetes
Mellitus
Early Onset Periodontitis
Localised Early Onset Periodontitis
Neutrophil Abnormality
Generalised Early Onset Periodontitis
Neutrophil Abnormality, Immunodeficient
Early Onset Periodontitis Related To Systemic Disease
LAD, Papillon-Lefevre Syndrome,Chediak Higashi Syndrome, AIDS,
Diabetes Mellitus Type I, Trisomy 21,
Early Onset Periodontitis, Systemic Determinants Unknown
Necrotising Ulcerative Periodontitis
Systemic Determinants Unknown
Related To HIV
Related To Nutrition
Periodontal Abscess

36. Modifications:
 Elimination of the ‘Refractory Periodontitis’
category - heterogeneous group
 Elimination of the ‘Periodontitis Associated with
Systemic Disease’ category
Shortcomings:
 Lenghty

37. AMERICAN ACADEMY OF PERIODONTOLOGY, 1999
GINGIVAL DISEASES
Dental plaque induced
Non plaque induced
CHRONIC PERIODONTITIS
Localised
Generalised
AGGRESSIVE PERIODONTITIS
Localised
Generalised
PERIODONTITIS AS MANIFESTATION SYSTEMIC DISEASES
Associated with hematological disorders
Associated with genetic disorders
Not otherwise specified

38. NECROTIZING PERIODONTAL DISEASES
Necrotizing Ulcerative gingivitis
Necrotizing Ulcerative periodontitis
ABSCESSES OF THE PERIODONTIUM
Gingival abscess
Periodontal abscess
Periocoronal abscess
PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS
Endodontic –periodontal lesion
Periodontal – endodontic lesion
Combined lesion
DEVELOPMENTAL OR ACQUIRED DEFORMITIES OR CONDITIONS
Localized tooth related
Mucogingival deformities around teeth
Mucogingival deformities in edentulous area
Occlusal trauma

39. GINGIVAL DISEASES
 Dental plaque induced gingival diseases:
1) Gingivitis associated with plaque only:
Without local contributing factors
With local contributing factors

42. 2) Gingival diseases modified by systemic factors
Puberty associated gingivitis
Menstrual cycle associated gingivitis
Pregnancy associated gingivitis
Diabetes mellitus associated gingivitis
3) Associated with blood dyscrasias
Leukemia associated gingivitis
Others

46. 4) Gingival diseases modified by medications
Drug influenced gingival enlargements
Drug induced gingivitis
5) Gingival diseases modified by malnutrition

49.  Non-Plaque-Induced Gingival Lesions
1. Gingival diseases
of bacterial origin
• Neisseria
gonorrhea-
associated lesions
• Treponema
pallidum-
associated lesions
• Streptococcal
species-associated
lesions
• Other
2. Gingival diseases
of viral origin
• Primary herpetic
gingivostomatitis
• Recurrent oral
herpes
• Varicella-zoster
infection
• Other
3. Gingival diseases
of fungal origin
• Candida-species
infections
• Histoplasmosis
• Other

50. 4. Gingival lesions of genetic origin
a. Hereditary gingival fibromatosis
b. Other

51. 5. Gingival manifestations of systemic conditions
A) Mucocutaneous disorders
i) Lichen planus
ii) Pemphigoid
iii) Pemphigus vulgaris
iv) Erythema multiforme
v) Lupus erythematosus
vi) Drug induced
vii) Other

52. B) Allergic reactions
Dental restorative materials
• Mercury
• Nickel
• Acrylic
• Other
Reactions attributable to
• Toothpastes/Dentifrices
• Mouthrinses/Mouthwashes
• Chewing gum additives
• Foods and additives
• Others

53. 6. Traumatic lesions
7. Foreign body reactions
8. Not otherwise specified (NOS)
Factitious Iatrogenic Accidental

54. CHRONIC PERIODONTITIS
 Localised
 Generalised

55. Clinical features and characteristics of
Chronic Periodontitis are:
 Most prevalent in adults
 Amount of destruction is consistent with the
presence of local factors
 Subgingival calculus is a frequent finding
 Variable microbial pattern
 Slow to moderate rate of progression

56.  Sub classifications:
Localised
(<30%)
Generalised
(>30%)
Slight
(1-2mm)
Moderate
(3-4 mm)
Severe
(≥ 5mm)

57.  Can be modified by :
Local factors
Environmental
factors
(smoking,
stress)
Systemic
factors
(diabetes
mellitus, HIV)

58. AGGRESSIVE PERIODONTITIS
 Localised
 Generalised

59. Common features of localized and generalized
forms of Aggressive Periodontitis are:
 Patients are otherwise clinically healthy
 Rapid attachment loss and bone destruction
 Familial aggregation.
 Amount of microbial deposits inconsistent with
disease severity

60. Common characteristics, but not universal:
 Diseased sites infected with A.a
 Abnormalities in phagocyte function
 Hyper-responsive macrophages producing
elevated levels of PGE2 and IL-1β
 Self-arresting disease progression

61.  Sub classifications
Localised
• Circumpubertal onset
• Localised proximal
attachment loss on at
least two permanent
teeth, one of which is
first molar
• Robust serum
antibody response
Generalised
• Usually , < 30 years
• Generalised proximal
attachment loss
affecting at least three
teeth other than first
molar and incisor
• Poor serum antibody
response

62. PERIODONTITIS AS A MANIFESTATION OF
SYSTEMIC DISEASE
Hematologic
• Neutopenias
• Leukemias
• Others
Genetic
• Cyclic neutropenia
• Down syndrome
• LAD syndrome
• Chediak –Higashi
Syndrome
• Papillon- lefevre
syndrome

63. NECROTIZING PERIODONTAL DISEASE
 Necrotizing ulcerative gingivitis (NUG)
 Necrotizing ulcerative periodontitis (NUP)

64.  Necrotizing ulcerative gingivitis
NUG
Bacterial etiology
Necrotic lesion
Pre disposing
factors
(stress, smoking,
immunosuppresion)
Contributing factor
(Malnutrition)

65.  Necrotizing ulcerative periodontitis
 NUP + HIV : 20.8 times more likely to have
CD4+ cell counts below 200 cells/mm3
 Probability of death within 24 months : 72.9%

66. ABSCESSES OF THE PERIODONTIUM
 Gingival abscess
 Periodontal abscess
 Pericoronal abscess

67. • Involves the marginal gingiva or interdental
papilla.
• Trauma, Foreign body impaction etc
Gingival
• Located contiguous to the periodontal
pocket that leads to destruction of PDL and
alveolar bone
• Moderate to deep pockets, Incomplete
calculus removal etc
Periodontal
• Within the tissue surrounding the crown of a
partially erupted tooth.
• Retention of debris, plaque etc beneath the
operculum
Pericoronal

68. PERIODONTITIS ASSOCIATED WITH
ENDODONTIC LESION
 Endodontic – Periodontal Lesion
 Periodontal – Endodontic Lesion
 Combined Lesion

69.  Endodontic – Periodontal L esion
Periapical lesion Accessory canals
Periodontal ligament PDL / Furcation
Clinical attachment
and bone loss
Pulpal infection

70. PERIODONTITIS ASSOCIATED WITH
ENDODONTIC LESION
 Endodontic – Periodontal Lesion
 Periodontal – Endodontic Lesion
 Combined Lesion

71. DEVELOPMENTAL OR ACQUIRED
DEFORMITIES OR CONDITIONS
 Localized tooth related
 Mucogingival deformities around teeth
 Mucogingival deformities in edentulous area
 Occlusal trauma

72. Localized tooth related factors
1)Tooth anatomic factors
2)Dental restorations/appliances
3)Root fractures
4)Cervical root resorption and cemental tears

73. • Cervical enamel projections and enamel pearls
• Palatogingival grooves, proximal root grooves
• Open contacts
Tooth
anatomic
factors
• Impingement of biologic width
• Rough surfaces
Dental
restorations
• Apical migration of plaque along fracture line
Root fractures

74. B) Mucogingival deformities and conditions
around teeth
1) Gingival/soft tissue recession
2) Lack of keratinized gingiva
3) Decreased vestibular depth
4) Aberrant frenum / muscle position
5) Gingival excess
a. Pseudopocket
b. Inconsistent gingival margin
c. Excessive gingival display
d. Gingival enlargement
6) Abnormal color

75. Mucogingival deformities and conditions on
edentulous ridges
1) Vertical and/or horizontal ridge
deficiency
2) Lack of gingival/keratinized tissue
3) Gingival/soft tissue enlargement
4) Aberrant frenum/muscle position
5) Decreased vestibular depth
6) Abnormal color

76. Occlusal trauma
1) Primary occlusal trauma
2) Secondary occlusal trauma

79. 1. Addition of a Section on "Gingival Diseases“
 Clinical expression of gingivitis can be substantially
modified by:
1) systemic factors
2) medications, and
3) malnutrition
 Non-plaque induced gingival lesions includes a wide
range of disorders that affect the gingiva.

80. 2. Replacement of "Adult Periodontitis" With
"Chronic Periodontitis“
 The age-dependent nature – diagnostic dilemma
 A nonspecific term : "Chronic Periodontitis" – more
accurate
 Substitute terminology
Periodontitis-
Common
Form
Type II
Periodontitis
Chronic
Periodontitis

81. 3. Replacement of "Early-Onset
Periodontitis" With "Aggressive
Periodontitis"
 Wise to discard classification terminologies
that were age-dependent or required
knowledge of rates of progression

82. 4. Elimination of a Separate Disease Category
for “Refractory Periodontitis”
 "Refractory Periodontitis" – not a single disease
entity.
 Small percentage of cases of all forms of
periodontitis might be non responsive to
treatment.
 The "refractory" designation - applied to all forms
of periodontitis in the new classification system
(e.g., refractory chronic periodontitis, refractory
aggressive periodontitis, etc.

83. 5. Clarification of the Designation
“Periodontitis as a Manifestation of Systemic
Diseases”
 Retained in the new classification since it is
clear that destructive periodontal disease can be
a manifestation of certain systemic diseases.
 It should be noted that diabetes mellitus is not
on this list.

84. 6. Replacement of “Necrotizing Ulcerative
Periodontitis” With “Necrotizing Periodontal
Diseases”
 Both clinical conditions under the single
category of "Necrotizing Periodontal Diseases."
 Inclusion of "Necrotizing Periodontal Diseases"
as a separate category is that both NUG and
NUP might be manifestations of underlying
systemic problems such as HIV infection.

85. 7. Addition of a Category on "Periodontal Abscess”
8. Addition of a Category on "Periodontic-
Endodontic Lesions”
9. Addition of a Category on "Developmental or
Acquired Deformities and Conditions”

86. MERITS:
 A gingivitis or gingival disease category
 Heterogeneous disease categories of prepubertal,
refractory and rapidly progressive periodontitis
eliminated.
 Criteria of age and rate of progression removed
 The reasons for these changes - not arbitrary, but
based on available data and understanding of the
nature of periodontal infections

87. Critical evaluation
 Complex classification as numerous disease categories
are listed
 Diabetes associated gingivitis and not Diabetes
associated periodontitis
 Developmental/ acquired deformities – Inappropriate to
include it
 Removal of localized juvenile periodontitis – retrograde
step, most well defined of all periodontal diseases and
with a large body of research

88.  Term ‘chronic’ as a replacement for ‘adult’ –
inappropriate
 Not based on the microbiological features or genetic
factors that control the clinical expression of these
diseases
 Chronic Periodontitis’ - polymicrobial and polygenic, are
altered by important environmental and host-modifying
conditions.
Hence, possible to subclassify the multiple forms of
‘Chronic Periodontitis’ into discrete microorganism/host
genetic polymorphism groups

89. Extent Severity Age
Clinical
characteristics
VAN DER VELDEN,
2005

92. Parameters are set in the following order: extent,
severity, clinical characteristics and age
Examples for diagnoses are:
 Generalized severe refractory post adolescent
periodontitis,
 Localized minor prepubertal periodontitis,
 Localized severe adult periodontitis.

93. Demerits
 Refractory periodontitis
 Modification by Systemic factors
 Gingival diseases

94. Conclusion
 Classification systems for periodontal diseases
have evolved based on the understanding of the
nature of these diseases
 Although classification systems for periodontal
diseases currently in use are based on, the
Infection/Host Response paradigm, some
features of the older paradigms are still valid and
have been retained.
 The new system is not perfect and will need to be
modified

95. References
 Gary C. Armitage, Classifying periodontal diseases – a
long standing dilemma., Periodontology 2000, Vol. 30,
2002, 9–23
 Gary C. Armitage, Periodontal diagnosis and
classification of periodontal diseases. Periodontology
2000, Vol 34, 2004, 9-21
 Gary C. Armitage, Development of a classification
system for periodontal diseases and conditions. Ann
Periodontol 1999;4:1-6.
 Ubele Van Der Velden, Purpose and problems of
periodontal disease classification. Periodontology 2000,
Vol. 39, 2005, 13–21
 Newman, Takei, Klokkevold, Carranza. 10th edition.

96. Thank you!