This document discusses the history and development of classification systems for periodontal diseases. It begins with early classification attempts in the late 19th century based primarily on clinical features. In the 1920-1970 period, classifications were dominated by the "classical pathology" paradigm focusing on non-inflammatory degenerative forms of periodontitis. Starting in the 1970s, the "infection/host response" paradigm emerged as the dominant view, recognizing periodontitis as inflammatory diseases caused by bacterial infection. The document reviews several influential classification systems developed under this new paradigm from the 1970s to present day.

1. CLASSIFICATION
SYSTEMS OF
PERIODONTAL DISEASES
Dr Manu Bhaskaran Nair

2. CONTENTS
• Introduction
• Characterstics of a classification system
• Need for a classification system
• Historical perspective
• Dominant paradigms in the development of periodontal
diseases
• Different classification systems
• References

3. INTRODUCTION
• Classification systems are used for most diseases and help
clinicians to design appropriate therapeutic strategies,
based on evidence from appropriately conducted clinical
trials.
• Classification of periodontal diseases is a subject of
inevitable controversy .
• The classification of periodontal diseases has come a long
way over the past hundred years.
• Periodontitis is a complex disease of the tooth supporting
structures resulting in inflammation in supporting tooth
structures resulting in progressive attachment loss and
bone loss that has no geographic , ethnic or age barriers.

4. • Disease classification is useful for the purpose of
diagnosis, prognosis and treatment planning.
• To provide maximum assistance in diagnosis &
treatment planning diseases have been classified
mainly on the basis of three criteria:
CLINICAL
FEATURES
PATHOLOGICAL
CHANGES
ETIOLOGY

5. • However, periodontal diseases cannot be classified
according to their aetiology because they are complex
diseases that are polymicrobial and
polyimmunoinflammatory in nature.

6. CHARACTERSTICS OF A
CLASSIFICATION SYSTEM
1. Should have a suitable organizing principle matching the
nature of the items being classified.
2. Every item should fall into atleast one of the classes
3. No item should fall into more than one of the classes
4. Should serve its users
5. Simpler the classification,easier for its rememberance and
application

7. NEED FOR A CLASSIFICATION
SYSTEM
To provide a foundation to study the etiology,
susceptibility traits, pathogenesis, and treatment
of diseases in an organized manner.
To give clinicians a way to organize the
health care needs of their patients.
Assemble similar disease phenotypes in
more homogeneous syndromes.
For diagnosis, prognosis and treatment planning,
Guide for clinical management of periodontal
problems.

8. HISTORICAL
PERSPECTIVE
•Girolamo Cardano is the
first person to differentiate
periodontal diseases.
Fauchard (1723)- Scurvy of the gums

9. • Early 19th century- Riggs disease
• Introduced by JohnW Riggs (1810-1885)
• Known as “Father of Periodontology”
RIGGS disease-loss of alveoli without
loss of gums
•Death of periodontal membrane
•Deprives the alveoli of nutrition
•Death of alveolar bone

10. DOMINANT PARADIGMS INTHE
HISTORICAL DEVELOPMENT OF
CLASSIFICATION SYSTEM
1870-1920
1920-1970
1970-the
present
CLINICAL FEATURESOF
DISEASES
CONCEPT OF CLASSIC
PATHOLOGY
INFECTIONAND HOST
RESPONSE PARADIGM

11. Clinical features of the disease
(1870-1920)
Classified entirely on the
basis of clinical
characterstics
Little knowledge about
etiology and pathology
Publications during the
time presented opinion of
a single person

12. John Riggs (1875)
margins of the gums showed inflammatory
action & bleeding at slightest touch of the brush.
inflammation extends over the thinner alveolar
border causing absorption of bone & gum tissue,
forming small pockets filled with pus
thicker portions of the process are involved
absorbing it most rapidly
the disease has swept away all of the alveoli &
much of the gum. John M. Riggs (1875)

13. • A paper was published by C.G. Davis in 1879 who
believed that there were three distinct forms of
destructive periodontal disease:
C.G DAVIS 1879
Gingival recession
with little or no
inflammation
Periodontal
destruction
secondary to lime
deposits
Riggs disease-
Hallmark of which is
loss of alveolus
without loss of gum
Davis apparently believed that
calculus exerted mechanical
pressure on the gingiva causing
the alveolar bone to resorb
because of lack of nutrition.

14. Limitations
1. No emphasis was given on age of onset of diseases
and rate of progression.
2. Inadequate or unclear classification criteria.
3. Little or no scientific evidence was used to support the
opinions of the clinicians of that time.
4. Periodontitis which can be due to systemic diseases is
not considered.

15. GV Black’s Classification (1886)
• Includes potassium iodide gingivitis
• ScurvyConstitutional
gingivitis
• a clinical condition that resembled
what is now termed necrotizing
ulcerative gingivitis (NUG), but he
never used the term
A painful form
of gingivitis
• associated with the accumulation of
debris that eventually led to ‘calcic ‘
inflammation of the peridental
membrane
Simple
gingivitis

16. • associated with ‘salivary’ and/or
‘serumal calculus.
• even or generalized pattern of
destruction of alveolar bone
• Destruction usually occurred slowly
• Black’s description fits the periodontal
disease that is now known as chronic
periodontitis.
Classic
inflammation
of the
peridental
membrane
• irregular pattern of destruction
• not much dental calculus
• In a later publication Black replaced
the term ‘phagedenic
pericementitis’ with ‘chronic
suppurative pericementitis’
phagedenic
pericementitis
(phagedenic
=spreading ulcer
or necrosis)

17. Limitations
• Little or no scientific evidence was used to
support the opinions of the clinicians of that
time.
• Inappropriate emphasis on age of onset of
diseases and rates of progression of this
diseases.
• Inadequate or unclear classification criteria.
• Periodontitis which can be due to systemic
diseases is not considered.

18. By 1929 one
author estimated
that there were ‘...
over 350 theories
of pyorrhea’ and
much confusing
terminology…..

19. Terminologies for Periodontitis
In the latter part of 19th century, the terms used were-
pyorrhea alveolaris
Riggs’ disease
calcic inflammation of the peridental membrane
phagedenic pericementitis
chronic suppurative pericementitis
During this period, the dominant term used for
destructive periodontal disease was pyorrhea alveolaris.(Toirez , 1779)

20. Classical pathology paradigm
(1920–1970)
• As the field of periodontology began to mature scientifically
in the first half of the 20th century, many clinical scholars in
both Europe and North America began to develop, and argue
about, nomenclature and classification systems for
periodontal diseases
• The concept was introduced by Gottlieb and Orban based on
the over-interpretation of histopathological studies.
• Two forms of destructive periodontal disease
Inflammatory
Non inflammatory
(‘degenerative’ or
‘dystrophic’)

21. • Gottlieb, in particular, had a significant influence on the
field when he postulated that “certain forms of
destructive periodontal disease were due to
degenerative changes in the periodontium”.
• He believed that he had discovered histological
evidence of an impairment in the continuous
deposition of cementum (i.e. ‘cementopathia’).
Later called as “PERIODONTOSIS”

22. • This cemental defect was presumably initiated by the
degeneration of the principal fibers of the periodontal
ligament that eventually resulted in detachment of
connective tissue from the tooth followed by resorption
of adjacent bone.
• Gottlieb’s ideas were probably widely accepted because
they appeared to explain the long-standing and
perplexing clinical observation –
• some young patients with relatively clean mouths had
massive and localized bone loss with only minimal or no
overt signs of gingival inflammation

23. • The profession was ready to embrace a plausible
etiological explanation for what would eventually be
called localized aggressive periodontitis.(Armitage et
al).
• Almost all classification systems from 1920–1970
included disease categories labeled as
‘dystrophic’,
‘atrophic’,
‘degenerative’

24. Mccall and Box 1925
• introduced the term ‘PERIODONTITIS’ for the Ist time
to denote those inflammatory diseases in which
gingiva, bone and PDL are involved.
• Based on systemic etiological factors-
1) Simplex periodontitis(exogeneous factors)
2) Complex periodontitis. (endogeneous factors)

25. Gottlieb’s classification
1928
• Schmutz-pyorrhea(poor oral
hygiene)
Inflammatory
• Diffuse alveolar atrophy(Systemic or
metabolic causes-non inflammatory)
• Paradental pyorrhea(Irregularly
distributed pockets)
Degenerative or
atrophic
• form of physical overload which was
believed to result in resorption of the
alveolar bone and loosening of teeth
Occlusal trauma

26. Limitations
• No microbial analysis.
• Inflammatory process is over interpretated as
degenerative process.
• Gingival diseases not included

27. Beck’s classification -1931
Paradentitis
(originates from the
gum disease in the
form of gingivitis)
Genuine
paradentosis
(originates in the bony
alveolus)

28. Orban 1942
• Classification systems of the period were dominated by
the ‘Classical Pathology’ paradigm which is based on
the ‘principles of general pathology’ as articulated by
Orban et al.
• First classification recognized by the American
Academy of Periodontology
• PERIODONTOSIS-to designate the ‘non-inflammatory
disease’ & was a separate distinct disease entity.

31. • Orban based this classification on a combination of his
perceptions of the etiologic,clinical, and pathologic
features of the diseases.
• He grouped them according to the ‘‘pathologic’’
categories of Inflammation, Degeneration, Atrophy,
Hypertrophy, andTraumatism.
Demerits
1. Degeneration is not an appropriate word to be used,
rather it should be called Inflammatory diseases.
2. Microbiological bases were not given much
importance

32. Other classifications (Classical
pathology paradigm)
• Fish – 1944
• Hine & Hine – 1944
• Lyons - 1946
• Coolidge & Hine – 1951
• Goldman et al – 1956
• Carranza -1959
• Wade – 1960
• Glickman-1964
• Goldman & Cohen – 1968
• Grant et al - 1968

33. 1. Almost all the classifications used from 1920-1970
included disease categories labeled as ‘dystrophic’,
atrophic or degenerative.
2. Classification system were dominated by the Classical
Pathology paradigm which is based on principles of
general pathology.
3. There was no scientific basis for retaining the concept
that there were non-inflammatory or degenerative
forms of destructive periodontal disease
DRAWBACKS FROM 1920-1970

34. During 1950 & 1960s the importance of dental plaque
as the major etiologic factor for periodontal diseases
became more and more evident.
The ultimate proof of association between plaque and
gingival inflammation was shown by Loe and
coworkers in their experimental gingivitis
studies(1965,1966)
In 1966 the workshop in periodontics concluded the
report: ‘Evidence to support the conventional concept
of periodontosis is unsubstantiated’

35. • The first generally acknowledged classification of
periodontal disease appeared in 1966 in Ann Arbor
(Michigan, USA) during the firstWorkshop, at which the
disease was classified into :
• “Gingivitis” and “Periodontitis”.
1966WorldWorkshop in Periodontics
•serious questions were raised about the existence of
‘periodontosis’ as a distinct disease entity
•Many in attendance at that meeting recommended
that the term be discarded.

36. • Information summarized at that meeting supported the
conclusion that ‘periodontosis’ was actually an
infection.
• Nevertheless, the committee is aware that some
evidence exists to indicate that a clinical entity different
from adult periodontitis may occur in adolescents and
young adults.
• Soon after the workshop a study was published by
Butler(1969) introducing the term
JUVENILE PERIODONTITIS instead of periodontosis.
Around 1970 a different paradigm (i.e. the ‘Infection/ Host Response
Paradigm’) had begun to dominate thoughts about the nature of periodontal
diseases.

37. INFECTION/HOST RESPONSE
PARADIGM(1970 to present)
Soon after the 1876 publication of Robert Koch in which he
provided experimental proof of the germ theory of disease,
some dentists began to suggest that periodontal diseases
might be caused by bacteria.(Harlan et al.)
•W.D. Miller , in particular, was an early proponent of the
infectious nature of periodontal diseases.

38.  Miller also recognized that certain systemic conditions
(e.g. diabetes, pregnancy) could modify the course of
disease.
 Although he spent most of his life studying the oral
microflora associated with caries and periodontal
disease, his work had very little impact on convincing
his contemporaries that periodontal diseases were
infections.
 He was, however, an early advocate of the
‘Infection/Host Response Paradigm’ that would come to
dominate the field nearly a hundred years later.

39. ‘In my opinion three factors are to be
taken into consideration in every case
of pyorrhea alveolaris: (1) predisposing
circumstances, (2) local irritation, (3)
bacteria. ‘... pyorrhea alveolaris is not
caused by any specific bacterium, which
occurs in every case ..., but various
bacteria may participate in it ...’
Ref -(MillerWD,The Micro-organisms of
the Human Mouth . Philadelphia:The
S.SWhite Dental Mfg.Co,1890:328-334)

40. • In addition, microbiological studies revealed that the
periodontal microflora was exceedingly complex and no
clear group of microorganisms could be causally linked to
the diseases.
• It was not until the classical ‘experimental gingivitis’
studies published by Harald Löe and his
colleagues from 1965 to 1968 that the
Infection/Host Response Paradigm
began to move in the direction of
becoming the dominant paradigm.

41. • The next major discovery in periodontal microbiology was
the preliminary demonstration in 1976–1977 of microbial
specificity at sites with periodontosis.
• This finding, coupled with the demonstration in 1977–
1979 that neutrophils from patients with juvenile
periodontitis (periodontosis) had defective chemotactic
and phagocytic activities .
• This marked the beginning of the dominance of the
Infection/Host Response paradigm.

42. Classifications under Infection/
Host response paradigm
 Goldman & cohen 1972
 Prichard – 1972
 American academy of Periodontology-1977
 Ramford & Ash – 1979
 Page & Schroeder - 1982
 American Dental Association – 1982
 Weatherford Classification -1987

43. • Suzuki’s Classification- 1988
• Grant, Stern, Listgarten, 1988
• WorldWorkshop in Clinical Periodontology – 1989 •
• Genco 1990
• Ranney’s Classification – 1993
• EuropeanWorkshop on Periodontics – 1993
• World workshop– 1999

44. AAP -1977
•Juvenile Periodontitis
•Chronic Marginal
Periodontitis
RAMJFORD & ASH -1979
GINGIVITIS
SIMPLEX
COMPLEX
TRAUMATIC
GINGIVAL
ATROPHY/RECESSION
TRAUMA FROM
OCCLUSION
PERIODONTITIS
SIMPLE
COMPLEX
SYSTEMIC
LOCAL

45. MERITS
1. simple & convenient way of categorizing periodontal
diseases.
2. Gingival atrophy or recession as a separate category.
DEMERITS
1. Periodontal abscess & perio-endo lesions not included.

46. PAGE&SHROEDER-1982
• Based on age, pocket flora, leukocyte function tests,
serum antibodies, clinical & radiographic pictures,
progression & history
PREPUBERTAL
PERIODONTITIS
JUVENILE
PERIODONTITS
RAPIDLY PROGRESSIVE
PERIODONTITIS
ADULTTYPE
PERIODONTITS

47. MERITS
• Simplified, convenient and uncomplicated.
• systemic & local factors.
• Age of onset is taken into consideration which is adopted in
subsequent classifications
• Designed to accommodate additional forms of diseases as
new insights are gained & additional forms are identified.
DEMERITS
• Gingival diseases not included.
• Non-validated age-dependent criteria.
• Periodontal Abscess not included.
• Periodontic-endodontic lesions not included.
• Occlusal trauma not included.

48. AMERICAN ACADEMY OF
PERIODONTOLOGY-1986
1. Juvenile Periodontitis
• Prepubertal periodontitis
• Localized juvenile periodontitis
• Generalized juvenile periodontitis
2. Adult periodontitis
3. Necrotizing Ulcerative Gingivo-Periodontitis
4. Refractory Periodontitis

49. Demerits
1. Absence of a gingival diseases component .
2. Periodontitis which can be due to systemic diseases has
not been considered .
3. Periodontal abscess and periodontic-endodontic lesions
were not included.
4. Extensive overlap among the categories.
5. Age dependent classification of periodontitis appears
invalid.

50. WORLD WORKSHOP AAP-
1989(California,USA)
• The next major landmark in the classification of
periodontal diseases emerged from the 1989World
Workshop in Clinical Periodontics.
• based on the Infection/ Host Response paradigm
• refinement of one that had been proposed by Page &
Schroeder in 1982 and a similar one that had been
adopted by the AAP in 1986

51. MERIT- depended heavily on the age of the patient and rates
of progression.

52. Drawbacks
1.Considerable overlap in clinical characteristics of the
different disease categories
2. Inappropriate emphasis on age of onset of disease and
rates of progression
3. Absence of a gingival disease component.
4. Rapidly progressive & prepubertal periodontitis and
refractory periodontitis were heterogenous category.
5.The 1989 classification did not include a section on the
connection between periodontitis and endodontic
lesions..

53. 1. Overlapping occurred among categories, and cases
existed that did not clearly fit into any single category.
For example,
if children with generalized prepubertal periodontitis have
defects in leukocyte adherence, could that justify their
inclusion in the category “periodontitis” as a
manifestation of systemic disease or generalized
prepubertal periodontitis?
2. Clear distinction between generalized juvenile
periodontitis and RPP in all cases is not yet possible
since these and other forms of early onset periodontitis
can be found in the same family.

54. 3. Inappropriate emphasis on age of onset of disease and rates
of progression.
Using the patient’s age as the major classification criterion
has important limitations since clinical conditions with the
same underlying etiology and susceptibility may be classified
differently on the basis of the patient’s age only.
4. Inadequate or unclear classification criteria.
For example,
• how does one classify the type of periodontal disease in a 21-
year- old patient with the classical
incisor-first molar pattern of
localized juvenile periodontitis (LJP)?
• Since the patient is not a juvenile,
should the age of the patient be ignored
and the disease classified as LJP anyway?

55. SoWHAT Next??....
• As a consequence of these problems, the 1989 classification
was criticized shortly after it was published and a different
system was proposed by Ranney in 1993.
• He suggested elimination of the ‘Refractory Periodontitis’
category since it was a heterogeneous group and it was
impossible to standardize the treatment that necessarily
would have to be given prior to making the diagnosis.
• He recommended elimination of the ‘Periodontitis
Associated with Systemic Disease’ category since the,
expression of all forms of periodontitis can be modified by
some systemic diseases or abnormalities,

56. RANNEY-1993
1.GINGIVITIS
• Gingivitis plaque induced
-systemically aggravated by sex hormones,drugs,systemic
diseases.
• NUG
-Systemic determinants unknown
-Related to HIV
• Gingivitis,non-plaque induced
-Assosciated with skin diseases like allergy and infections

57. 2.PERIODONTITIS
• Adult periodontitis
- Non-aggravated
-Systemically aggravated
• Early-onset periodontitis
- Localised / generalized
-Related to systemic diseases
-Systemic determinants unknown
• NUP
-Systemic determinants unknown
-Related to HIV
-Related to nutrition
• Periodontal abscess

58. MERITS
• This system includes not only forms of gingivitis &
Periodontitis other than those caused by plaque but also
modifying factors, for ex. Systemic aggravating factors,
general diseases status, viral infections & so on.
DEMERITS
• Trauma from occlusion factor was not considered.
• Periodontic-endodontic lesions were not included.
• Term adult periodontitis created a diagnostic dilemma
for clinicians, needed to be replaced with term chronic.

59. • SO AGAIN A CLASSIFICATION SYSTEM WAS
PROPOSED IN 1993 BY EUROPEAN WORKSHOP IN
PERIODONTOLOGY. (ATTSTROM &VANDER
VELDEN)
• Adult Periodontitis - Begins at the 4th decade of life,
slow rate of progression of disease.
• Early onset Periodontitis - Begins before the 4th
decade of life, rapid rate of progression of disease,
altered host response is seen.
• Necrotizing Periodontitis -Tissue necrosis with clinical
attachment and bone loss is seen.

60. Elaboration of the broad spectrum of
periodontal diseases encountered in clinical
practice was absent in the 1993 European
classification.
during the 1996WorldWorkshop in
Periodontics, the need for a revised
classification system for periodontal
diseases was stressed.
In 1997, the American Academy of
Periodontology responded to this need and
formed a committee to plan and organize an
international workshop to revise the classification
system for periodontal diseases.
The InternationalWorkshop for a
Classification of Periodontal Diseases and
Conditions was held and a new classification
was agreed upon in 1999.(Oct 30-Nov 2)

61. CONCLUSION
• Classification of periodontal diseases has
proved to be problematic.
• Over the period, clinicians and researchers have been wrestling
around with the problem and
• Have been assembling periodically to review or develop the
classification of various forms of periodontal disease as
research have expanded our knowledge of these diseases.
• This has resulted in frequent revisions and changes
• A classification however should not be regarded as a permanent
structure.
• It must be adaptable to change and evolve with the
development of new knowledge.
• It is thus expected that classification systems would change
over time.

62. Next seminar-
• 1999 AAP classification
• Key changes to the Periodontal Classification
system(Add-ons & Eliminations)
• The newly proposed 2017 classification system
• Conclusion
• References

63. References
• The Periodontal Disease Classification System of the
American Academy of Periodontology — An Update,Colin et
al
• Development of a Classification System for Periodontal
Diseases and Conditions Gary C. Armitage
• Development and Evolution of Classification of Periodontal
Diseases: An Insight ,Dr. Mahajan Aaditi, Dr. Kolte Rajashri
Dr. Kolte Abhay
• Classifying periodontal diseases – a long-standing
dilemma,Perio2000,volume30
• Periodontal diseases: a brief historical
perspective,Perio2000,vol2 HARALLDo E
• Carranza 12th edition
• Google Images

64. CLASSIFICATION SYSTEMS
OF PERIODONTAL
DISEASES-II
Dr Manu Bhaskaran Nair

65. TO BRUSH UP……..
• Characterstics and the need for the classification
system
• Clinical characterstic paradigm(1870-1920)
• Classical Pathology paradigm(1920-1970)
• Infection & Host Response Paradigm(1970-present)
• Classifications that eventually led to 1999 American
academy of Periodontology Classification System

66. CONTENTS
• 1999 AAP classification
• Key changes to the Periodontal Classification
system(Add-ons & Eliminations)
• The newly proposed 2017 classification system
• Conclusion
• References

67. WHERE WERE WE
TILLTODAY???
• The AAP and European classification schemes were
further amended in 1999 when –
• The International Workshop forClassification of
Periodontal Diseases was convened to address a
number of issues that were felt to be lacking in the 1989
and 1993 classifications.
• Till today we were strictly following the 1999
Classification of Periodontal diseases.

68. CHANGES INTHE CLASSIFICATION
SYSTEM FOR PERIODONTAL
DISEASE
ADDITION OFA SECTION ON “ GINGIVAL DISEASES”
REPLACEMENT OF “ADULT PERIODONTITIS” WITH
“CHRONIC PERIODONTITIS”
REPLACEMENT OF “EARLY ONSET
PERIODONTITIS” (EOP)WITH “AGGRESSIVE
PERIODONTITIS” (AP)
ELIMINATION OFA SEPARATE DISEASE CATEGORY
FOR “REFRACTORY PERIODONTITIS” (RP)

69. CLARIFICATION OFTHE DESIGNATION “PERIODONTITIS AS A
MANIFESTATION OF SYSTEMIC DISEASES”
REPLACEMENT OF “NECROTIZING ULCERATIVE
PERIODONTITIS(NUP)WITH “NECROTIZING PERIODONTAL
DISEASES” (NPD)
ADDITION OF A CATEGORY ON “PERIODONTAL ABSCESS”
ADDITION OF A CATEGORY ON “PERIODONTIC ENDODONTIC
LESIONS”
ADDITION OF A CATEGORY ON “DEVELOPMENT OR ACQUIRED
DEFORMITIES AND CONDITIONS”

73. This is an extremely complex classification
with over 100 disease categories listed and,
owing to its complexity.
it is unrealistic for general
practitioners to use
thus, to allow ease of understanding and clinical
application, the classification has been
simplified to the main subcategories of the 1999
classification.

76. Let’s go slightly in depth……
1. ‘Aggressive Disease’ in place of ‘Early-onset Periodontitis’
• In the 1999 classification, ‘aggressive disease’ was defined as
disease in patients who were systemically healthy, had rapid loss
of attachment and alveolar bone, and a high incidence of a
familial link.
• is useful as it addresses the clinical behavior of the disease but
avoids the controversial age barrier.
• Clearly, older subjects can experience episodes of more rapid
attachment loss; whilst this is rare ,it is embraced by the new
system.
• However, it is accepted that most patients falling into this
category will be less than 30 years old.

77. 2. ‘Chronic Periodontitis’ Instead of ‘Chronic Adult Periodontitis’
• In the 1999 classification, ‘chronic periodontitis’ was subdivided into
localized and generalized on the basis of the number of sites
affected, localized being up to 30% of sites, and generalized being
more than 30% of sites.
• 1999Workshop suggested that the severity of disease could be
categorized on the basis of clinical attachment loss (CAL):
• Slight: CAL 1–2 mm.
• Moderate: CAL 3–4 mm.
• Severe: CAL 5 mm or more.
• Traditionally, the term ‘adult periodontitis’, used by previous
classification systems, relates to patients over the age of 35 years,
and approximately 16% of the population over this age will have
disease.
• However, it is important to note that adolescents also suffer from
slowly progressive attachment loss; hence chronic disease.

78. 3. Addition of a ‘Gingival Disease’ Category
• important inclusion in the classification.
• split into ‘plaque-induced’ and ‘nonplaque- induced’
gingival diseases, although a number of conditions causing
non-plaque-induced disease are not included.

79. 4. Removal of ‘Refractory Disease’ as aTerm
Refractory disease can be defined by the 1989
classification as continued loss of attachment despite
the provision of adequate treatment and the patient
maintaining a good level of oral hygiene.
1999Workshop considered that ‘refractory disease’ was
not a separate disease entity, suggesting that any
periodontal disease could be termed ‘recurrent disease’
(‘recurrent aggressive periodontitis’, ‘recurrent chronic
periodontitis’, etc.).

80. 5. Sub classification of ‘Periodontal Disease as a
Manifestation of Systemic Disease’
‘ periodontitis associated
with systemic disease’
(1989)
‘periodontal disease as
a manifestation
of systemic disease’.
(1999)
This is really misnamed, as the conditions
listed are strictly systemic diseases that
affect the periodontal tissues, or present
within them, rather than periodontal
diseases arising denovo.
Diabetes mellitus has not been included in
this subclass as it can modify all forms of
periodontal disease, and there is insufficient
information to conclude that there is a
specific diabetes mellitus-associated form of
periodontitis.
same reasoning is
applied to smoking,
which is therefore also
not included because it
is considered a
significant modifier of
all periodontal diseases.

81. 6. Replacement of ‘ANUG’ and ‘ANUP’
with ‘Necrotizing Periodontal Diseases’
• The workshop agreed that ANUG and ANUP were clinically
distinguishable disease entities, although they were
unsure whether they were two separate diseases or part of
the same disease process.
• insufficient evidence to warrant two separate categories
and the term ‘necrotizing periodontal diseases’ was
introduced.
• 1999 classification omitted ‘acute necrotizing stomatitis’
which would have been a useful inclusion.

82. 7. Addition of ‘Periodontal– Endodontic Lesions’
The 1989 classification did not include
this group, and this was amended in
1999 to include only one category: the
‘combined lesion’.
This had been recommended in an earlier
publication(Chapple ILC, Lumley PJ.The
periodontal endodontic interface. Dent
Update 1999)
Was welcomed because it implied a
single treatment regimen based on the
pathology present and not on the
aetiology of the lesion

83. 8.Addition of Category on ‘Developmental or Acquired
Deformities and Conditions’
This category is difficult to interpret
and it seems inappropriate to include
it in a classification of periodontal
diseases as the conditions within this
group are modifying factors.
These factors alter susceptibility to
disease rather than being discrete
disease entities.
For example, primary occlusal trauma is a condition, whereas secondary occlusal
trauma refers to the modification of the persisting periodontitis by excessive occlusal
forces.

84. 9. Removal of ‘Localized Juvenile Periodontitis’
• The removal of this diagnostic category from the
classification systems is unfortunate because localized
juvenile periodontitis is the most well defined of all
periodontal diseases.
• Features include-
• a strong association with Acetomyces
actinomycetemcomitans;
• reduced chemotactic and phagocytic activity of the host’s
polymorphonuclear cells;
• strong family history, suggesting a genetic association.
These factors in our view make
the loss of this particular term
from the international
language of periodontology a
retrograde step.

85. DRAWBACKS
• It is an extremely complex classification with over 100
disease categories listed and, owing to its complexity, its
clinical application is difficult.
• Periodontal diagnosis around implants were not included
• No research revealed specific bacterial characteristic in AP(
Kinane & Attstrom, 2002)
• It does not solve the problems as how severe a case must be
in order to be classified as AP.
• Knowledge about the rate of progression is still needed.
• The use of AP implies that the person is systemically healthy
but has periodontal diseases. But is not seen in all cases.

86. ESSENTIALISTIC OR NOMINALISTIC
DISEASES CLASSIFICATION-
(VANDERVELDON,2000)
According to Sherp in 1964- one obvious problem is
that one of the most important components of
periodontitis is expressed in all patients in the same
way, i.e. the amount of loss of attachment.
Essentialistic idea implies the real existence of a
disease caused by a class of agents.
Since periodontitis is a syndrome, present & future
classification have to be based on nominalistic
concept.

87. Classification based on this should be
• Simple to apply.
• Not susceptible to multiple interpretations.
• Determined on the basis of documented differences regarding the
consequences of the diagnosis.
At present a classification which comes closest to these principles was
published byVan derVelden in 2000.
Based on
a) Extent
b) Severity
c) Age
d) Clinical characteristics.
Ideally, a nominalistic disease definition describes a set of criteria that
are fulfilled by all persons said to have the disease, but not fulfilled by
persons that are considered free from the disease

92. So how is the classification
established??
•First, the extent category is
determined by counting the
number of teeth with the most
severe condition
•Second, the severity category is
determined for each tooth
•Diagnosis on the basis of clinical
characteristics is added if
applicable
•Diagnosis on the basis of age
localized minor pre-
pubertal periodontitis
localized severe
juvenile periodontitis
semi-generalized minor
juvenile periodontitis
generalized severe
refractory post-adolescent
periodontitis

93. Update of AAP 1999 to be
revised in 2017
• The Academy announced that an update to the 1999
Classification would commence in 2017.
• Three specific areas of concern:-
• ATTACHMENT LEVEL
• CHRONIC versus AGGRESSIVE PERIODONTITIS
• LOCALIZED versus GENERALIZED PERIODONTITIS

94. 2017 classification
system-The present!!
• A classification scheme for periodontal and peri‐implant
diseases and conditions is necessary for clinicians to
properly diagnose and treat patients as well as for
scientists to investigate etiology, pathogenesis, natural
history, and treatment of the diseases and conditions.
• The workshop was co‐sponsored by the American
Academy of Periodontology (AAP) and the European
Federation of Periodontology (EFP) and included expert
participants from all over the world.
• held in Chicago on November 9 to 11, 2017

95. PERIODONTAL DISEASESAND
CONDITIONS
Periodontal health,
gingival diseases and
conditions
Periodontitis
Other conditions
affecting periodontium
1.Periodontal Health
& Gingival Health
2.Gingivitis :
Dental bio film
induced
3.Gingival diseases :
Non dental biofilm
induced
1.Necrotizing
Periodontal
diseases
2.Periodontitis
3.Periodontitis as
a manifestation
of systemic
disease
1.Systemic diseases or
conditions affecting the
periodontal supporting
tissues.
2.Periodontal abcess
&endo perio lesion
3.Mucogingival
deformities and
conditions
4.Traumatic occlusal
forces
5.Tooth & prosthetic
related factors

96. Peri-Implant Diseases and Conditions
Peri-implant health Peri-implant mucositis Peri-implantitis
Peri-implant
soft&hard tissue
deficiencies

97. PERIODONTAL HEALTH , GINGIVITIS ,
AND GINGIVAL CONDITIONS
1.Periodontal health and gingival health(Lang&Bartold 2018)
a)Clinical gingival health on an intact periodontium
b)Clinical gingival health on a reduced periodontium
i)Stable periodontitis patient
ii)Non-periodontitis patient
bleeding on probing should be the primary parameter
to set thresholds for gingivitis

98. 2.Gingivitis:Dental biofilm induced(Murakami et al 2018)
a)Assosciated with dental biofilm alone
b)Mediated by systemic or local risk factors
c)Drug influenced gingival enlargement
3.Gingival diseases:Non-dental biofilm induced(Holmstrup et al
2018)
a)Genetic/developmental disorders
b)Specific infections
c)Inflammatory and immune conditions
d)Reactive processes
e)Neoplasms
f)Endocrine,nutritional&metabolic diseases
g)Traumatic lesions
h)Gingival pigmentatiion

99. Periodontitis was further characterised based on multidimensional staging
and grading system-
STAGING-
• largely dependent upon the severity of disease at presentation as well as
on the complexity of disease management.
GRADING-
• provides supplemental information about biological features of the
disease,
• history based analysis of the rate of disease progression,
• assessment of the risk for further progression,
• Anticipated poor outcomes of treatment
• assessment of the risk that the disease or its treatment may negatively
affect the general health of the patient.
NOTE- Patient with gingivitis can revert to a state of health,
but a periodontitis patient remains a periodontitis patient for
life, even following successful therapy, and requires life‐long
supportive care to prevent recurrence of disease.

100. FORMS OF PERIODONTITIS
1.Necrotizing Periodontal diseases(Herrera et al,2018)
• Nectrotizing gingivitis
• Necrotizing periodontitis
• Necrotizing stomatitis
2.Periodontitis as a manifestation of systemic
disease(Jepsen,Caton et al,2018) (Albandar et al 2018)
• It is recognized that there are rare systemic disorders, such as
Papillon Lefèvre Syndrome, that generally result in the early
presentation of severe periodontitis.
• Such conditions are grouped as “Periodontitis as a
Manifestation of Systemic Disease”, and classification should
be based on the primary systemic disease.

101. So the question of diabetes??
• These appear to be part of the multifactorial nature of
complex diseases such as periodontitis and are included in
the new clinical classification of periodontitis as a descriptor
in the staging and grading process.
• Although common modifiers of periodontitis may
substantially alter disease occurrence, severity, and response
to treatment, current evidence does not support a unique
pathophysiology in patients with diabetes and periodontitis.
(Sanz et al. Scientific evidence on the links between
periodontal diseases and diabetes: consensus report and
guidelines of the joint workshop on periodontal diseases and
diabetes by the International Diabetes Federation and the
European Federation of Periodontology.)

102. 3.Periodontitis(Fine et al,2018) (Needleman et al 2018)
(Billings et al,2018)
a)Stages : Based on severity and complexity of management
Severity-interdental CAL at sites with greatest loss,
radiographic bone and tooth loss
Complexity of management-Probing depth, pattern of bone
loss,furaction lesions, number of remaining teeth, tooth
mobility, ridge defects, masticatory dysfunction
Stage I-Initial Perodontitis
Stage II-Moderate periodontitis
Stage III-Severe periodontitis with potential for additional
tooth loss
Stage IV-Severe periodontitis with potential for loss of
dentition

103. b)Extent and distribution-
i-Localised (<30% teeth)
ii-Generalised (>30% teeth)
iii-molar incisor distribution
c)Grades-Evidence or risk of rapid progression(direct evidence by
periapical radiographs or CAL loss or indirect boneloss/age
ratio) and anticipated treatment response(case phenotype ,
smoking,hyperglycemia)-
i)Grade A-Slow rate of progression
ii)Grade B-Moderate rate of progression
iii)Grade C-Rapid rate of progression
PLUS POINT – Grading allows the clinician to include individual
patient factors into the diagnosis, which are crucial to
comprehensive case management

104. PERIODONTAL MANIFESTATIONS OF
SYSTEMIC DISEASES AND DEVELOPMENTAL
AND ACQUIRED CONDITIONS
(Jepsen,Caton et al 2018)
1.Systemic diseases or conditions affecting the
periodontal supporting tissues(Albandar et al)
2.Other Periodontal conditions(Papanou,Sanz et al 2018)
(Herrera et al 2018)
a)Periodontal abcesses
b)Endodontic Periodontal lesions

105. 3.Mucogingival deformities and conditions around
teeth(Cortellini&Bissada 2018)
• Gingival phenotype
• Gingival/soft tissue recession
• Lack of gingiva
• Decreased vestibular depth
• Aberrant frenum/muscle position
• Gingival excess
• Abnormal colour
• Conditons of exposed root surface

106. 4.Traumatic occlusal forces(Fan &Canton 2018)
• Primary occlusal trauma
• Secondary occlusal trauma
• Orthodontic forces
5.Prosthesis and tooth related factors that modify or
predispos to plaque induced gingival
diseases/periodontitis (Ereoli&Caton 2018)
• Localized tooth related factors
• Localized dental prosthesis-related factors

107. CHANGES INTHE CLASSIFICATION OF
PERIODONTAL DEVELOPMENTAL
AND ACQUIRED DEFORMITIES AND CONDITIONS
Mucogingival conditions
new case definitions related to treatment of gingival recession are
based on
• interproximal loss of clinical attachment
• assessment of the exposed root and cemento‐enamel junction.
new classification of gingival recession that combines clinical
parameters including the
• gingival phenotype
• characteristics of the exposed root surface
.
periodontal biotype was replaced by periodontal
phenotype

108. Occlusal trauma and traumatic occlusal forces
• Traumatic occlusal force, replacing the term excessive
occlusal force, is the force that exceeds the adaptive
capacity of the periodontium and/ or the teeth.
• result in occlusal trauma (the lesion) and excessive wear
or fracture of the teeth
Prosthesis‐ and tooth‐related factors
• expanded in the new classification.
• term biologic width was replaced by supracrestal
attached tissues.
• Clinical procedures involved in the fabrication of indirect
restorations was added because of new data indicating
that these procedures may cause recession and loss of
clinical attachment

109. PERI-IMPLANT DISEASES AND
CONDITIONS
(Berglundh,Armitage et al 2018)
1.Peri-implant health(Araujo & Lindhe 2018)
2.Peri implant mucositis(Heitz-Mayfield & Salvi
2018)
3.Peri implantitis(Schwarz et al 2018)
4.Peri implant soft and hard tissue
deficiencies(Hammerie&Tarnow 2018)

110. 1.Peri implant health
• Clinically, peri‐implant health is characterized by an
absence of visual signs of inflammation and bleeding on
probing
• Peri‐implant health can exist around implants with
normal or reduced bone support.
• not possible to define a range of probing depths
compatible with peri‐implant health.

111. 2.Peri-implant mucositis
• characterized by bleeding on probing and visual signs of
inflammation.
• Peri-implant mucositis-strong evidence that is caused
by plaque
• Non-plaque induced-Limited evidence
 Peri‐implant mucositis can be reversed with measures
aimed at eliminating the plaque.

112. 3. Peri-implantitis
“defined as a plaque‐associated pathologic condition occurring
in the tissue around dental implants, characterized by in the
peri‐implant mucosa and subsequent progressive loss of
supporting bone”.
• Peri‐implant mucositis is assumed to precede peri‐implantitis
• associated with poor plaque control and with patients with a
history of severe periodontitis
• onset of peri‐implantitis may occur early following implant
placement as indicated by radiographic data
• Peri‐implantitis, in the absence of treatment, seems to
progress in a non‐linear and accelerating pattern

113. 4.Hard and soft tissue implant site deficiencies
Tooth loss Normal healing
Diminished
dimension of
alveolar
process/ridge
Soft and hard
deficiencies
Larger ridge deficiencies can occur –
•sites associated with severe loss of periodontal support
extraction trauma, endodontic infections.
•root fractures, thin buccal bone plates, poor tooth position,
injury and pneumatization of the maxillary sinuses.
•associated with medications and systemic diseases reducing
the amount of naturally formed bone, tooth agenesis, and
pressure from prostheses.

114. QUESTIONS &
ANSWERS OF
INTEREST
1. Should diabetes‐associated periodontitis be a distinct diagnosis?
• Ans-There are no characteristic phenotypic features that are unique to
periodontitis in patients with diabetes mellitus.
• On this basis diabetes‐associated periodontitis is not a distinct disease
• diabetes is an important modifying factor of periodontitis, and should be
included in a clinical diagnosis of periodontitis as a descriptor.
• There is mounting evidence of specific mechanistic pathways in the
pathogenesis of periodontitis in patients with diabetes.
• In a more etiologically driven classification this should require further
consideration in the future

115. 2. Should smoking‐associated periodontitis
be a distinct diagnosis?
• Ans-Although tobacco use was once classified as a habit, it is
now considered a dependence to nicotine and a chronic relapsing
medical disorder (International Classification of Diseases,Tenth
Revision).
• There are no unique periodontal phenotypic features of
periodontitis in smokers.
• On this basis smoking‐associated periodontitis is not a distinct
disease
• Tobacco smoking is an important modifying factor of
periodontitis, and should be included in a clinical diagnosis of
periodontitis as a descriptor.
• According to the new classification of periodontitis,the current
level of tobacco use influences the grading of periodontitis.

116. GINGIVAL RECESSION
• It is proposed to adopt a classification of gingival recession
with reference to the interdental clinical attachment loss
1. RecessionType 1 (RT1): Gingival recession with no loss of
interproximal attachment. Interproximal CEJ is clinically not
detectable at both mesial and distal aspects of the tooth.
2.RecessionType 2 (RT2): Gingival recession associated with
loss of interproximal attachment. The amount of
interproximal attachment loss (measured from the
interproximal CEJ to the depth of the interproximal
sulcus/pocket) is less than or equal to the buccal attachment
loss (measured from the buccal CEJ to the apical endof the
buccal sulcus/pocket).
3.RecessionType 3 (RT3): Gingival recession associated with
loss of interproximal attachment. The amount of
interproximal attachment loss is higher than the buccal
attachment loss

117. 3. Can traumatic occlusal forces cause gingival
recession?
• There is evidence from observational studies that
occlusal forces do not cause gingival
recession.(Bernnimoilin(1977),Harrel et al(2005)
• 4. What is the biologic width?
• Biologic width is a commonly used clinical term to
describe the apico‐coronal variable dimensions of the
supracrestal attached tissues.
• The supracrestal attached tissues are histologically
composed of the junctional epithelium and supracrestal
connective tissue attachment.
• The term biologic width should be replaced by
supracrestal tissue attachment.

118. 5.Which criteria would need to be fulfilled to support the
contention that chronic and aggressive periodontitis are
indeed different diseases? (e.g., etiology, histology,
pathophysiology, clinical presentation, other)
• Differences in etiology and pathophysiology are required to
indicate presence of distinct periodontitis entities; variations
in clinical presentation per se, i.e. extent and severity, do not
support the concept of different diseases
6. Does current evidence suggest that we should continue to
differentiate between “aggressive” and “chronic”
periodontitis as two different diseases?
• Current evidence does not support the distinction between
chronic and aggressive periodontitis, as defined by the 1999
Classification Workshop, as two separate diseases
• however, a substantial variation in clinical presentation
exists with respect to extent and severity throughout the age
spectrum, suggesting that
• there are population subsets with distinct disease trajectories
due to differences in exposure and/or susceptibility.

119. 7. How do we define a patient as a periodontitis case?
• In the context of clinical care, a patient is a
“periodontitis case” if:
• Interdental CAL is detectable at ≥2 non‐adjacent teeth,
• Buccal or oral CAL ≥3 mm with pocketing ≥3 mm is
detectable at ≥2 teeth

120. Evidence b/w chronic & aggressive
periodontitis
• three position papers that are relevant to the discussion
of aggressive and chronic periodontitis.-
Fine,Needleman &Billings)
no evidence of specific pathophysiology that enables
differentiation of cases that would currently be
classified as aggressive and chronic periodontitis or
provides guidance for different interventions.
little consistent evidence that aggressive and chronic
periodontitis are different diseases, but there is
evidence of multiple factors, and interactions among
them, that influence clinically observable disease
outcomes (phenotypes) at the individual level..

121. On a population basis, the mean rates of
periodontitis progression are consistent across all
observed populations throughout the world.
There is evidence, however, that specific segments
of the population exhibit different levels of disease
progression, as indicated by greater severity of
clinical attachment loss (CAL) in subsets of each age
cohort relative to the majority of individuals in the
age cohort.
classification system based only on disease severity
fails to capture important dimensions of an
individual's disease, including the complexity that
influences approach to therapy, the risk factors that
influence likely outcomes, and level of knowledge
and training required for managing the individual
case.

122. In the past, characterizations of the aggressive
forms of periodontitis have been limited by-
1.Low number of individuals who have this form of
disease
2.Inconsistency resulting from broad definitions
proposed in the past.
Choosing a new definition should not only be based on clinical
observation, like usual medical and dental history,clinical
charting,radiographic examinations,but should focus on
• phenotypic indicators such as age of onset
•location of lesions in defined populations.

123. CONCLUSION
• Since the 1999 workshop, substantial new information has
emerged from population studies, basic science
investigations, and the evidence from prospective studies
evaluating environmental and systemic risk factors.
• In the last 30 years, the classification of periodontitis has
been repeatedly modified in an attempt to align it with
emerging scientific ev idence.
• The workshop agreed that, consistent with current
knowledge on pathophysiology, three forms of periodontitis
can be identified: necrotizing periodontitis, periodontitis as a
manifestation of systemic disease and the forms of the
disease previously recognized as “chronic” or “aggressive”,
now grouped under a single category, “peri odontitis”.

124. An insight into the future!!
• Research into the aetiology and natural history of the
periodontal diseases is moving forward rapidly.
• It should be remembered that all classification systems
have their faults, and this may always be the case for
periodontal diseases, owing to their multifactorial origin
and varied natural history.
• The facility to study gene expression and the genetic
factors underlying the differences in host response to
periodontal pathogens between patients may help
inform the classification systems.

126. REFERENCES
• The Periodontal Disease Classification System of the AmericanAcademy of
Periodontology — An Update,Colin et al
• Development of a Classification System for Periodontal Diseases and
Conditions Gary C. Armitage
• Classification of Periodontal Diseases:Where were we?Where are we now?
Where are we going? M.R. Milward and i.L.C.Chapple
• Purpose and problems of periodontal disease classification Ubele van der
velden
• 2 017WORLDWORKSHOP Periodontal manifestations of systemic diseases
and developmental and acquired conditions: Consensus report of workgroup 3
of the 2017WorldWorkshop on the Classification of Periodontal and
Peri‐Implant Diseases and Conditions
• A new classification scheme for periodontal and peri‐implant diseases and
conditions – Introduction and key changes from the 1999 classification
• Periodontitis: Consensus report of workgroup 2 of the 2017WorldWorkshop on
theClassification of Periodontal and Peri‐ Implant Diseases and Conditions
• Staging and grading of periodontitis: Framework and proposal of a new
classification and case definition
• Classifying periodontal diseases – a long-standing Dilemma Development of a
Classification System Periodontal Diseases and Conditions Gary C. Armitage
• Google images