Classification of diseases and conditions affecting the periodontium

Classification of diseases
and conditions affecting
the periodontium
Copyright ©2021 Periowiki.com
Classification of diseases and

CONTENTS
- Introduction
- The need for periodontal classification system
- Dominant paradigms in the historical development of
classification systems
-Clinical characteristics paradigm :
(i) C. G Davis (1879)
(ii) G.V. Black (1886)
-Classical pathology paradigm :
(i) Gottlieb (1923)
(ii) Orban classification (1942)

-Infection/host response paradigm :
(i) Page & Schroeder classification (1982)
(ii) Suzuki classification (1988)
(iii) Grant, Stern & Listgarten classification (1988)
(iv) Johnson et al. (1988)
(v) Evolution of the AAP periodontal disease classification system
 Shortcomings of the 1989 classification system
(vi) Ranney Classification – 1993
(vii) European Classification in Periodontics-1993
(viii) The 1999 Classification system
 Shortcomings of the 1999 classification system
(ix) Classification for insurance purpose
(x)Vander velden 2000

- 2017 World Workshop on the Classification of Periodontal and Peri-
Implant Diseases and Conditions
- Future challenges in the classification system
- Conclusion
- Bibliography

Introduction
Our understanding of the etiology and pathogenesis of oral diseases & conditions
is continually changing with increased scientific knowledge.
In light of this, a classification can be most consistently defined by the
differences in the clinical manifestations of diseases and conditions because
they are clinically consistent and require little, if any, clarification by scientific
laboratory testing.
(Carranza’s clinical periodontology : 10th edition)

Related terms
Diagnosis is defined as the act of identifying a
disease from its signs and symptoms.
Classification is defined as the act or method of
distribution into groups.

Need for periodontal classification system
To provide a framework, so as to
scientifically study the etiology,
pathogenesis and treatment of
diseases in an orderly fashion.
To give clinicians a way to
organize the health care needs
of their patients
Direct research aimed at
learning more about the
diseases concerned
To help determine the
evidence base for better-
targeted therapy
To guide in public health
planning and targeting of
therapy.
Help practitioners plan
treatment protocols to
maximize benefit to all their
patients

“Periodontal disease classifications
are useful to help establish diagnosis,
determine prognosis, and facilitate
treatment planning.”
Michael G. Newman

History
The first classification system for periodontal disease
was recorded in 1806 when Joseph Fox attempted to
classify “gum- disease”
Alphonse Toirac in 1823 called it Pyorrhea Alveolaris

Dominant paradigms in the historical development
of classification systems
Clinical characteristics
paradigm
(1870–1920)
Classical pathology paradigm
(1920- 1970)
Infection/host response
paradigm
(1970 to present)

Clinical characteristics paradigm (1870–1920)
Features
1. No generally
accepted
terminology or
classification system
for periodontal
diseases was
adopted in this era
2. Very little was
known about the
etiology &
pathogenesis of the
periodontal diseases
3. Basis for
classification was:
clinical
characteristics
supplemented by
unsubstantiated
theories about their
cause
4. During this period,
the dominant term
used for destructive
periodontal disease
was “pyorrhea
alveolaris”
Riggs’ disease’ , ‘calcic
inflammation of the
peridental membrane’ ,
‘phagedenic
pericementitis’, and
‘chronic suppurative
pericementitis’

5. Main debates about the nature of periodontal diseases was whether they
were caused by local or systemic factors or both …!!!
Local factors
• Black GV (1894), Harlan AW (1883), Miller WD (1890), Patterson JD (1885),
• Rehwinkel FH (1877), Riggs JM (1882), Talbot ES (1886), Younger WJ (1894).
Systemic
factors
• Dunbar LL (1894), Mills GA (1881)
• Peirce CN (1892 & 1894)
Local +
systemic
factors
• Miller WD (1890), Talbot ES (1886)
• Patterson JD (1888 & 1891)

6. Classifications proposed :-
C. G. Davis (1879)
Gingival recession with
minimal or no
inflammation- this is due
to feeble vascular action
and trauma from tooth
brushing or other sources
Periodontal destruction
secondary to lime
deposits
Riggs disease : the
hallmark of which being
the loss of alveolus
without the loss of gum
A.

B. G.V. BLACK (1886)
Constitutional gingivitis-
including mercurial
gingivitis,potassium iodide
gingivitis and scurvy.
A painful form of gingivitis-
Black described a clinical
condition that resembled
what is now termed
necrotizing ulcerative
gingivitis (NUG),
Simple gingivitis- This was
associated with the
accumulation of debris that
eventually led to ‘calcic
inflammation of the
peridental membrane.’
Calcic inflammation of the
peridental membrane- This
was associated with
‘salivary’ and/or ‘serumal’
calculus
Phagedenic pericementitis-
(phagedenic = spreading
ulcer or necrosis).

Classical pathology paradigm
(1920- 1970)
Inflammatory
2 types of periodontal disease presentations
Non-
Inflammatory
Hunter laid the basis for a controversy, which remained central to periodontology for
almost two centuries: Inflammatory or degenerative?

Mc call and Box(1925):
Introduced the term
periodontitis - gingiva+
bone+ PDL involved by
inflammation
Simple periodontitis :
Due to local etiologic
factors
Complex periodontitis:
Due to systemic
etiologic factors
Sub-classifications
based on the
presumed etiologic
factors

The concept being periodontal diseases were caused by non-
inflammatory or degenerative processes
Gottlieb (1923)
Thoma KH,
Goldman HM
(1937)
Orban B (1942)

• Thought to be the result of the accumulation
of deposits on the teeth and was
characterized by inflammation, shallow
pockets, and resorption of the alveolar crest.
Schmutz- Pyorrhoe
• Described as a noninflammatory disease
exhibiting loosening of teeth, elongation,
and wandering of teeth in individuals who
were generally free of carious lesions and
dental deposits
Alveolar atrophy or
diffuse atrophy
• Characterized by irregularly distributed
pockets varying from shallow to extremely
deep. This form of disease may have started
as Schmutz-Pyorrhoe or as diffuse atrophy.
Paradental-Pyorrhoe
• Form of physical overload which was believed
to result in resorption of the alveolar bone and
loosening of teeth.
Occlusal trauma
Gottlieb in 1920s classified periodontal disease into 4 types

Gottlieb
1923
Described and gave
the term “ the
diffuse atrophy of
the alveolar bone”
1928
Gave the term “
deep
cementopathia”

Various changes with the periodontal terms
Author Year Terms introduced Features
Becks 1931 Made a distinction between
paradentitis, a disease which originates
from the gum tissue in the form of
gingivitis and genuine paradentosis,
which originates in the bony alveolus,
perhaps in the form of an osteopathy.
Wannenmacher 1938 Parodontitis
marginalis
progressive
Described incisor- first molar
involvement
Thoma KH,
Goldman HM
1940
Periodontosis
Considered a degenerative , non-
inflammatory disease process
Orban B,
Weinmann JP
1942
Goldman HM 1947

Classification
proposed by:
Orban (1942)

The committee on nomenclature of the AMERICAN ACADEMY OF
PERIODONTOLOGY IN 1949 defined periodontosis as a
“ a degenerative non inflammatory destruction of the periodontium
originating in one or more of the periodontal structures , characterized by
migration and loosening of the teeth in the presence or absence of
secondary epithelial proliferations and pocket formation or secondary
gingival disease’’.
The term ‘periodontosis’ is controversial term , and there are some
periodontists who denied the existence of this disease entity

Based on a literature review covering the period from Gottlieb’s 1920
paper, the 1951 Workshop on Periodontal Disease concluded that “It
appears from the evidence to be found in the literature that
periodontosis does exist as an entity …”
In the early 1960‟s, the well-known experimental gingivitis studies of Löe and
coworkers established that accretion of dental plaque results in gingivitis and that
gingivitis can be treated by means of plaque removal. These results were seen
to deliver the final proof of the relationship between poor oral hygiene and
periodontitis.
At the time of the 1966 Workshop in Periodontics it was agreed that the term
periodontosis should be eradicated from the periodontal nomenclature, due to the
lack of evidence to support the concept of degeneration .Even so, the committee of
the meeting maintained the idea that a clinical entity different from adult
periodontitis may occur in adolescents and young adults.

1967 – Chaput and colleagues
1969 - Butler
1971 - Baer defined – juvenile periodontitis
“as a disease of the periodontium occuring in an otherwise
healthy adolescent which is characterized by a rapid loss of
alveolar bone about more than one tooth of the permanent
dentition, & the amount of destruction manifested is not
commensurate with the amounts of local irritants”.
There are two basic forms in which it occurs –
1. Only teeth affected are the first molars and incisors
2. Generalized form may affect most of the dentition

Infection/host response paradigm
(1970 to present)
1876 Robert koch - provided experimental proof of the germ theory of disease ,
some dentists began to suggest that periodontal diseases might be caused by
bacteria
W.D. Miller - “ …. pyorrhea alveolaris is not caused by any specific bacterium, which
occurs in every case..., but various bacteria may participate in it…” .
Three factors are to be taken into consideration in every case of pyorrhea alveolaris :
i. Predisposing circumstances
ii. Local irritation
iii. Bacteria

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.
Novel microbiological and histological methods were used to investigate
periodontal lesions, and one set of evidence against the periodontosis
concept was provided by Waerhaug who examined teeth extracted from
supposed cases of periodontosis.
These studies showed that subgingival dental plaque does play a role as a
cause of periodontosis and Waerhaug therefore suggested the replacement
of the name periodontosis with highly destructive juvenile periodontitis
when referring to this disease. (Waerhaug J. Plaque control in the treatment of juvenile
periodontitis. Journal of Clinical Periodontology. 1977;4(1):29-40.)

Lehner et al. 1974 The microbiological observations were coupled with
the suggestion made by Lehner et al and later reported
by others that juvenile periodontitis might also differ
from adult periodontitis by the presence of a selective
cell-mediated immunodeficiency
Newman et al
(1976, 1977)
Major discovery – preliminary demonstration of
microbial specificity at sites with periodontosis.
Genco, Lavine
(1977- 1979)
Neutrophils from patients with juvenile periodontitis
(periodontosis) had defective chemotactic and
phagocytic activities, marked the beginning of the
dominance of the Infection/Host Response paradigm.
Newman M, Socransky S.
(1977)
These investigators reported the presence of certain
capnophilic gram-negative microorganisms, and
anaerobic rods in cases of periodontosis/juvenile
periodontitis, indicating that “some or all of these
organisms play a significant role in the initiation and or
progression of the pathologic process in periodontosis”.

Defined periodontitis as an inflammatory disease of the
periodontium characterized by the presence of periodontal pockets
and active bone resorption with acute inflammation.
Page & Schroeder classification (1982)
Generalized & Localized

Features Prepubertal periodontitis Juvenile periodontitis
Age range Under 14 years Between 12- 26 years
Gender predilection Males = Females Females more than males
Forms Localized &
Generalized -----
Clinical
presentation
First molar & incisor
involvement, lack of clinical
inflammation with
presence of deep pockets
- Depressed neutrophil
chemotaxis
- Genetic implications
- Possible medical
considerations
-Depressed neutrophil
chemotaxis
- Genetic implications
- Possible medical
implications
- AMLR slightly increased

“Pre-pubertal periodontitis”

“Rapidly progressing periodontitis”
Age of onset is between
puberty and 35
Lesions are generalized,
affecting most of the teeth,
without any consistent
pattern of distribution
Some, but not all, patients
may have had juvenile
periodontitis
Microbial deposits highly
variable
During active phase-
acutely inflamed gingiva &
arrested phase-the tissues
appear free of
inflammation
Severe and rapid bone
destruction, after which
the destruction process
may cease spontaneously
or greatly slow
Functional defects in
neutrophils or monocytes
Systemic manifestations-
weight loss, mental
depression & general
malaise

“Adult periodontitis”
Patients over
35 years of age
Approximately
equal sex
distribution
Plaque &
calculus
present
Host-response
apparently
normal
Genetic
implications
unknown.

Classification systems proposed in 1988
(i) SUZUKI’s CLASSIFICATION
Suzuki stated that ‘ Additional clinical observations , based
on factors such as age, microbial deposits and the autologous
mixed lymphocyte reaction, rapidly progressing periodontitis
can be subdivided into type A and type B.
 In addition, the term post juvenile periodontitis delineated
a slow progression –type of juvenile periodontitis.

“Rapidly progressing periodontitis”
Sr. Type A Type B
1. 14 & 26 yrs of age Over 26 years of age
2. Females affected more than
males (2:1 to 3:1)
Sex distribution not established
3. Generalized lesions Generalized lesions
4. Minimal tooth-associated
materials
Minimal tooth-associated materials
5. Plaque & calculus present
6. Caries rate variable Caries rate variable
7. Depressed neutrophil chemotaxis Neutrophil chemotaxis depressed or
normal
8. Depressed AMLR AMLR within normal limits
9. Genetic implications Genetic implications not known
10. Possible medical considerations Possible medical considerations

- Patients generally between 26 &35 yrs of age
- Females affected more than males(3:1)
- First molar and incisor lesions
- Plaque and calculus present
- Caries rate variable
- Neutrophil function
- AMLR slightly increased
- Genetic implications not known
“Post juvenile periodontitis”

(ii) Johnson et al Classification (1988)
“Proposed a classification, in which clinical features, such as age, intra-oral
distribution and rate of progression, formed the sole basis for the distinction
between the entities”.

(iii) Grant, Stern & Listgarten Classification (1988)
Bacterially induced
diseases
Functionally induced
diseases
Trauma
Gingivitis
Traumatic occlusion Habits
Periodontitis
(i) Adult type
(ii) Postjuvenile
(iii) Early onset
a. Juvenile
- Localized
- Generalized
Disuse atrophy Accidents
ANUG
Acute abscess
Pericoronitis
(8th edition Carranza )

Evolution of the AAP periodontal disease classification system
From 1977 to 1989, the American Academy of
Periodontology (AAP) went from 2 main periodontal disease
categories to 5.
The 1989 periodontal disease classification was a significant
improvement over previous classifications.
In particular, the effect of systemic disease on periodontal
health was recognized and added as a category. Also, more
criteria for early onset diseases were added. Ex: Down syndrome,
Diabete type I, Papillon Lefevre syndrome

The 1989 classification had its shortcomings including:
(i) Lack of a category for strictly gingival diseases
(ii) Overlap between disease categories; difficulty in
fitting certain patients into any of the existing
categories
(iii) Similarity of microbiological and host response
features in reportedly different disorders;
(iv) An emphasis on age of onset that became a problem
as patients aged into a new category

Prepubertal
periodontitis
In retrospect, many of the
patients in the original
publication on this disease
category turned out to
have either
hypophosphatasia or
leukocyte adherence
deficiency (LAD) .
It is likely that most prepubertal
children with severe periodontal
destruction affecting the deciduous
teeth probably have a systemic
disease that increases their
susceptibility to bacterial infections
such as: LAD ,congenital primary
immunodeficiency, chronic neutrophil
defects and cyclic neutropenia.

Since there are no definitive answers to these, and other similar questions, the
classification lost some of its clinical utility.
The uncertainty about the
proposal that ‘Rapidly
Progressive Periodontitis’
was a single entity.
The questionable criteria
used to determine its
presence
To be designated as ‘rapid’,
how much progression has
to occur and over what
time period?
Can it be assumed from a
single examination that an
adolescent or young adult
with massive attachment
loss has this disease?
How can a clinician
distinguish between
‘Generalized Juvenile
Periodontitis’ and ‘Rapidly
Progressive Periodontitis’?
“Rapidly progressive periodontitis”

Topic B classification (1990)
Shortly after the 1989 World Workshop in Clinical Periodontics, Topić proposed a
classification which essentially tried to amalgamate all previous classifications.

Genco classification (1990)
Periodontitis in Adults
Periodontitis in juveniles
-Localized form
- Generalized form
Periodontitis with systemic involvement
-Primary neutrophil disorders
-Secondary or associated neutrophil
involvement
-Other systemic diseases
Miscellaneous conditions

Ranney classification (1993)
Refractory periodontitis
category be eliminated since
it was a heterogeneous group
and it was impossible to
standardize treatment
Recommended the elimination
of the ‘Periodontitis associated
with systemic disorders’
category since the expression
of all forms of periodontitis is
affected by systemic diseases.
The 1989
classification
was criticized
and a new
system of
classification
was proposed
by Ranney in
1993.

I. GINGIVITIS
A.
B.
1. Sex-hormone-related
2. Drug-related
3. Systemic-disease-related
C.
1. Dermatologic-disease-
associated
2. Allergic
3. Infective
D.
1. Systemic determinants
unknown
2. HIV-related

The European Workshop in Periodontics Classification
(1993)
The recommendation was that classification should be
based on causative factors and host-response factors

Problems, inconsistencies, and deficiencies associated with the 1989 classification led
many clinicians and investigators to call for a revision of the system and these
problems were addressed in 1999 world workshop.
The group recommended that the term “early-onset periodontitis” be discarded since
this term is too restrictive.
It was noted that features of this form of periodontitis can occur at any age and the
disease is not necessarily confined to individuals under the arbitrarily chosen age of
35 years.
The heterogeneous disease categories of prepubertal and rapidly progressive
periodontitis were eliminated as distinct or stand-alone entities.
Arbitrarily changed the names of ‘Juvenile Periodontitis’ to ‘Aggressive
Periodontitis.’ These changes were specifically made to eliminate the non validated
age-dependent designations.
1999 – World workshop

Changes in the
periodontal
classification
system
Addition of a
gingival disease
component
Replacement of “Adult
Periodontitis’’ with “Chronic
Periodontitis”
Elimination of “Refractory
Periodontitis” as a separate
entity
The term “early-onset
periodontitis” be
discarded since this
term is too restrictive
Arbitrarily changed the names of
‘Juvenile Periodontitis’ to
‘AggressivePeriodontitis.’ These
changes were specifically made to
eliminate the nonvalidated age-
dependent designations.
Sub classification of
“Periodontitis as a
manifestation of systemic
diseases.
Replacement of ANUG and
ANUP with Necrotizing
periodontal diseases.
Addition of category for
-Periodontal abscesses
-Periodontic - Endodontic
Lesion
- Acquired deformities &
conditions

The AAP International Workshop for Classification of Periodontal Diseases (1999)

DENTAL PLAQUE INDUCED
GINGIVAL DISEASES

Result of interaction between the
microorganisms found in the dental
plaque biofilm and tissues +
inflammatory cells of the host
Gingivitis associated with dental plaque only
Without local
contributing factors
With local
contributing factors
Local factors are contributory because
of their ability to retain plaque
microorganisms & inhibit their removal
by patient initiated plaque control
techniques

Gingivitis diseases modified by systemic factors
A. Endocrine system related Features
1. Puberty –associated gingivitis Frank signs of gingival
inflammation in the presence of
relatively small amounts of
plaque during the circumpubertal
period
2. Menstrual cycle associated
gingivitis
-Increase in the gingival exudate
by 20% during ovulation.
-However, changes in the
crevicular fluid flow are not
observable, hence not
accompanied by notable gingival
changes

• Increased propensity
to develop frank signs
of gingival
inflammation in the
presence of relatively
little plaque
Pregnancy
associated
gingivitis
• prevalence 0.5 to 5.0%
of pregnant women
• Common in maxilla in
the interdental space,
developing as early as
1st trimester
Pregnancy
associated
pyogenic
granuloma
3.

4. Diabetes
mellitus associated
gingivitis
Most commonly
associated with
children with poorly
controlled type I DM
Features similar to plaque
induced gingivitis except that the
level of diabetic control is more
of an important aspect than
plaque control in the severity of
the gingival inflammation
B. Leukemia associated
gingivitis
Common sign – gingival bleeding ( in
17.7% & 4.4% of patients with acute
& chronic leukemias)
Gingival enlargement reported to
initially begin at the interdental
papilla followed by marginal and
attached gingiva

Gingival diseases modified by medication
Drug induced gingival enlargements
Common clinical characteristics of
Drug induced gingival
enlargements include a variation
in the interpatient or intrapatient
pattern of enlargement
(i.e. genetic predisposition)
Oral contraceptive associated gingivitis
1. Plaque present at gingival margin
2. Pronounced inflammatory response of gingiva
3. Change in gingival colour
4. Change in gingival contour with possible
modification of gingival size
5. Increased gingival exudate
6. Bleeding upon provocation
7. Reversible following discontinuation of oral
contraceptives

Gingival diseases modified by malnutrition
Ascorbic acid deficiency gingivitis
Features of gingival lesions:
-Bulbous
- Spongy
- Hemorrhagic
- Swollen
- Erythematous

NON- PLAQUE INDUCED
GINGIVAL LESIONS

Gingival lesions of specific bacterial origin
Lesions occur when non-
plaque related pathogens
overwhelm innate host
response
Examples :
Infections with
Neisseria gonorrhoea
Treponema pallidium
Streptococci
Manifest as: fiery red,
edematous , painful
ulcerations

Gingival lesions of specific viral origin
Forms of Herpes virus infections:
1. Primary herpetic gingivostomatitis
2. Recurrent intraoral herpes
3. Varicella Zooster infections

Gingival lesions of specific fungal origin
1. Most frequently occurs in immunocompromised
individuals and those with normal flora disturbed by
the long term use of broad-spectrum antibiotics.
2. Generalized candidal infection may manifest as white patches on gingiva, tongue
or oral mucous membrane, that can be removed with gauze, leaving red bleeding
surface.
3. Individuals infected with HIV , candidal infection may present as erythema of the
attached gingiva and is referred to as linear gingival erythema or HIV – associated
gingivitis.

Gingival lesions of genetic origin
Hereditary gingival fibromatosis

Gingival manifestations of systemic conditions
Mucocutaneous
lesions
Allergic
reactions

Lichen planus
Pemphigoid
Pemphigus vulgaris
Erythema multiforme
Lupus erythematosus
Drug induced
Mucocutaneous
lesions

Allergic
reactions
1. Dental restorative
materials
- Mercury
- Nickel
- Acrylic
- Other
2. Reactions attributable to:
- Toothpaste or dentrifice
- Mouth rinses or
mouthwashes
- Chewing gum additives
- Food & additives

Traumatic lesions (factitious, iatrogenic, accidental)
• Surface itching due
to toxic products
• Incorrect use of
caustics by the
dentist
Chemical
• superficial gingival
lacerations
• gingival recession
• Gingivitis artefacta
Physical • Painful , red & may
slough the
coagulated surface
• Vesicles may occur
Thermal

Foreign body reactions
Leads to localized inflammatory
conditions of the gingiva
Amalgam introduction
into the gingiva during
restoration placement
Introduction of
abrasives into the
gingiva during polishing
procedures

Replacement of “Adult Periodontitis” with “Chronic Periodontitis”
Clearly, the age-dependent nature of the adult periodontitis
designation created problems.
Substitute terminology such as “Periodontitis— Common Form” and
“Type II Periodontitis” were considered and eventually rejected by the
majority of the group.
The term “Chronic Periodontitis” was criticized by some participants,
since “chronic” might be interpreted as “noncurable” by some people.
Nevertheless, “Chronic Periodontitis” was eventually agreed upon as
long as it was understood that it did not imply that this disease was
nonresponsive to treatment.

Clinical features and characteristics of chronic periodontitis
(G.Armitage)
1.Most prevalent in adults but can also occurs in children and adolescents.
2.Amount of destruction is consistent with the local factors
3.Sub gingival calculus is a frequent finding
4.Slow to moderate rate of progression but may have periods of rapid progression.
5.Can be associated with local predisposing factors (ex-Tooth related, Iatrogenic factors)
6.Associated with variable microbial pattern.
7.May be modified by and or associated with systemic diseases & environmental factors
such as cigarette smoking and emotional stress.
8. Can further be classified on the basis of extent & severity.
Extent – localized or generalized
Severity – slight: 1-2mm CAL
moderate: 3-4mm CAL
severe: >5mm CAL

Replacement of “Early-Onset Periodontitis” with “Aggressive Periodontitis”
- Workshop participants decided that it was wise to discard classification terminologies
that were age-dependent or required knowledge of rates of progression.
- Accordingly, highly destructive forms of periodontitis formerly considered under “Early-
Onset Periodontitis” were renamed using the term “Aggressive Periodontitis.” In general,
patients who meet the clinical criteria for LJP or GJP are now said to have “Localized
Aggressive Periodontitis” or “Generalized Aggressive Periodontitis,” respectively.
- The Rapidly Progressive Periodontitis (RPP) designation has been discarded. Patients who
were formerly classified as having RPP will, depending on a variety of other clinical criteria,
be assigned to either the “Generalized Aggressive Periodontitis” or “Chronic Periodontitis”
categories.
- Workshop participants agreed that prepubescent children who have periodontal
destruction without any modifying systemic conditions would, depending on a variety of
secondary features, fit under the categories of “Chronic Periodontitis” or “Aggressive
Periodontitis” in the new classification.

FEATURES COMMON TO PATIENTS
WITH AGGRESSIVE PERIODONTITIS
(LANG et al 1999)

Secondary features that are generally,
but not universally present are:
Elevated proportions of Aggregatibacter actinomycetemcomitans & in some
populations Porphyromonas gingivalis may be elevated
Phagocyte abnormalities
Hyper responsive macrophage phenotype including elevated levels of PGE2
and IL-1beta
Progression of attachment loss and bone loss may be self-arresting
Amounts of microbial deposits are inconsistent with the severity
of periodontal destruction

- Circumpubertal onset.
- Robust serum antibody response to infection.
- Localized 1st molar-incisor presentation with interproximal attachment loss on at
least 2 permanent teeth, one of which is the 1st molar & involving no more than 2
teeth other than 1st molars & incisors.
Localized aggressive periodontitis features

Generalized aggressive periodontitis features
Pronounced
episodic nature
of destruction
Poor serum
antibody
response to
infecting agents

Clarification of the Designation “Periodontitis as a Manifestation of
Systemic Diseases”
The term “periodontitis as a manifestation of systemic diseases’’ is a misnomer as the
conditions listed are strictly systemic diseases that affect the periodontal tissues.
The correct term should have been ‘periodontal manifestations of systemic disease’.
Diabetes mellitus has not been included in this category as it can modify all forms of
Similarly, the new classification does not contain a separate disease category
for the effects of cigarette smoking on periodontitis. Smoking was considered to be a
significant modifier of multiple forms of periodontitis.

Hematological disorders
Leukemia
-Frequently associated with acute form
- Generalized gingival enlargement in conditions
such as leukocyte adhesion deficiency (LAD)

Genetic disorders
Cyclic neutropenia. A 5-year-old boy. Features : the
very inflamed, erythematous and oedematous
gingiva, anterior migration, the advanced
premature exfoliation that is apparent and
the generalized severe bone loss on the radiograph.
Down syndrome. Features: the gingival
inflammation, splayed teeth and
macroglossia. The radiograph shows
severe bone loss.

Replacement of “Necrotizing Ulcerative Periodontitis” With “Necrotizing
Periodontal Diseases”
Since there are insufficient data to resolve these issues, the group
decided to place both clinical conditions under the single category of
“Necrotizing Periodontal Diseases.”
One of the potential problems with 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.

Diagnostic criteria
NUG NUP
Punched out ulcerated
papillae
Gingival bleeding
Pain
Deep interdental craters with
denudation of interdental
alveolar bone.
Sequestration of interdental
and possibly buccal and /or
lingual alveolar bone.

Addition of a Category on “Periodontal Abscess”
It could be argued that periodontal abscesses are part of the
clinical course of many forms of periodontitis and
formation of a separate disease category is not justified.
However, in the view of workshop participants, since
periodontal abscesses present special diagnostic and treatment
challenges they deserve to be classified apart from other

Gingival
abscess Periodontal
abscess
Pericoronal
abscess

Addition of a Category on “Periodontic Endodontic
Lesions”
Endodontic-
periodontal
lesion
Combined
lesion
Periodontal-
endodontic
lesion

Addition of a Category on “Developmental or
Acquired Deformities and Conditions”
Although the deformities and conditions listed in this section of the
classification are not separate diseases, they are important modifiers of
the susceptibility to periodontal diseases or can dramatically influence
outcomes of treatment.
Rationale for classification:
1. Clinical
2. Morphological
3. Severity
4. Etiologic

Elimination of “Refractory Periodontitis” category
•Refractory periodontitis refers to continued attachment loss in
spite of adequate treatment.
•The term recurrent periodontitis is now used to refer to the
return of periodontitis and not as a separate disease.
•Potentially any patients with a past history of periodontitis can
develop recurrent periodontitis if adequate oral hygiene is not
maintained.

“Shortcomings of 1999 classification”
Very long & extensive
Removal of the term “Localized juvenile periodontitis” is the
most unfortunate because it is the most clearly defined of
all periodontal diseases.
There is no provision for the category of “Historical or
“previous disease” for a patient who has suffered periodontal
disease in the past and is no longer currently active.

The developmental & acquired conditions/deformities
are not strictly periodontal conditions.
NUG & NUP together called as necrotizing periodontal
diseases, they should remain as separate terms.
The term ‘necrotizing stomatitis’ does not appear in the
necrotizing periodontal diseases list.

Classification for insurance purpose (1997)
For administrative and third-party insurance reporting
purposes, the American Academy of Periodontology classifies
gingivitis and periodontitis into five broad case types (1997).
CASE TYPE I - Plaque-associated gingivitis
CASE TYPE II - (early periodontitis) is characterized by
progression of inflammation into the deeper periodontal
structures with slight bone and attachment loss.

•CASE TYPE III (moderate periodontitis) is classified as a more
advanced state with increased destruction of the periodontal
structures and noticeable loss of bone support, possibly
accompanied by increased tooth mobility and furcation involvement.
•CASE TYPE IV (advanced periodontitis) is characterized by further
progression of periodontitis with major loss of alveolar bone support
that is usually accompanied by an increase in tooth mobility.
Furcation involvement is a common finding.
• CASE TYPE V (refractory periodontitis) includes those patients that
continue to demonstrate attachment loss after good conventional
therapy.

Essentialistic or nominalistic disease classification
The
essentialistic
concept The nominalism
concept

Scadding et al. - supported the nominalistic concept and stated
that the name of diseases are a convenient way of
stating concisely the endpoint of a diagnostic process
that advances from assessment of symptoms and signs
towards the knowledge of causation.
At present, the best option is to classify the periodontitis
syndrome in an exhaustive but also exclusive way and use a
terminology for the various classes of the disease which makes
it easy to understand the case. A classification which comes
closest to these principles was recently published by Van der
Velden (2000).

Vander Valden Classification (2000)
Stated that : that previous classifications suffer from the central problem that
they are “susceptible to multiple interpretations”.

Based on Extent

Based on severity

Based on age

Based on clinical characteristics

2017 World Workshop on the Classification of Periodontal and
Peri-Implant Diseases and Conditions

What are the primary differences between the 1999 and the 2018 classifications
of periodontitis?
1. According to the 1999 classification, chronic and aggressive periodontitis
were considered to represent different disease entities.
However, research conducted since then failed to document
sufficiently distinct biologic features between the two diseases; therefore, in
the new classification, they have been regrouped under the single term
“periodontitis.”
2. 1999 classification placed emphasis on disease severity and used the
designations of slight, moderate, and severe periodontitis. The diagnosis
could be divided into severity levels in different parts of the mouth.
For example, a patient might have generalized moderate chronic
periodontitis with localized severe periodontitis.
Over the past several decades, it is confirmed that a diagnosis based
on severity alone represents a one-dimensional view of a complex disease.

What are the primary differences between the 1999 and the 2018 classifications
of periodontitis?
3. 2018 classification, which introduces the concept of staging, supports a
multidimensional view of periodontitis, incorporating severity, tooth loss due
to periodontitis, and complexity of management of the patient’s periodontal
and overall oral rehabilitation needs. Staging is based on a full-mouth
diagnosis; it cannot be subdivided into different severity levels.
4. Grading incorporates additional biological dimension of the disease, including
history-based and/or anticipated rate of periodontitis progression, presence
and control of risk factors, and the potential impact of periodontitis on
general health.
Once the stage and grade are determined, they become the “guiding
stars” for difficulty of treatment, prognosis for the dentition, and
expectations during maintenance therapy.

Is the intent of staging and grading to arrive at a diagnosis that will drive
treatment? Why should I change to staging periodontitis? What important
diagnostic information do stage and grade convey?
Staging and grading do not help the practitioner arrive at a diagnosis.
A diagnosis of periodontitis is determined first, with staging and grading providing
supplemental information.
Staging and grading help clarify extent, severity, and complexity of the patient’s
condition as well as the potential rate of disease progression, predicted response
to standard therapies, and potential impact on systemic health.
They also encompass other aspects of periodontitis including pattern of bone
loss, tooth loss, furcation status, treatment difficulty, prognosis for tooth loss, and
degree of restorative difficulty and complexity.

How do I apply extent/distribution?
Once the stage is determined then the percentage of teeth affected by
periodontitis is assessed.
This provides information about how many teeth are affected by periodontitis,
which is expressed as localized or generalized.
It does not give information about the percentage of teeth with slight,
moderate, or severe destruction.
Distribution refers to affected teeth, such as first molars and/or incisors, which
is a totally different type of clinical presentation that should be noted and may
have treatment implications.

Can I use a stage for each quadrant or sextant like I did with a severity-based
diagnosis of slight, moderate, or severe?
No. Staging is designed to give information about the whole mouth, relative to
the severity and complexity.
The stage will also inform the clinician of the initial difficulty and complexity of
required treatment as well as expected prognosis since it provides some
perspective on the individual patient’s response to the disease challenge at the
time of the examination.
For example, a patient in his 30s or 40s with past destruction and case
complexity consistent with Stage III or IV should be considered very differently
than a patient with Stage I or II disease and complexity.

Does the area with the most severe destruction determine the stage?
Yes. The staging system is designed to highlight the patient’s most severe
areas of destruction, which usually require more complex case management.
For example, when a patient has periodontitis with a combination of
generalized mild (CAL 1-2 mm, PD ≤4 mm) to moderate destruction (CAL 3-4
mm, PD ≤5 mm) and localized severe destruction (CAL ≥5 mm, PD ≥6 mm), he/
she would be given a diagnosis of Generalized Periodontitis: Stage III or
possibly IV if ≥5 teeth are missing due to periodontitis.

If a patient is missing teeth due to periodontitis and the clinician must extract
additional teeth due to periodontitis, do these teeth also count as being lost to
periodontitis?
Yes. In the staging table, tooth loss is defined as “tooth loss due to periodontitis.”
Tooth loss should include those teeth planned for extraction due to periodontitis
as part of active therapy.
For example, if a patient diagnosed with periodontitis had previously lost two
teeth due to periodontal disease and he/she now has an additional three teeth
that clearly require extraction due to periodontal destruction, those teeth
planned for extraction should be included in the count of teeth “lost due to
periodontitis.”
Thus, the patient would have five teeth lost due to periodontitis and would be
classified as Stage IV.

Why do I need to utilize grading?
Grading provides the likelihood of post-treatment disease progression. It is
loosely based on previous clinical studies from private practices that classified
post-treatment status as Well Maintained, Downhill, or Extreme Downhill, based
on the amount of post-treatment tooth loss.
The designations recommended are A, B, or C, signifying slow or no progression,
moderate progression, and rapid progression, respectively. The assessment is
based on past progression, presence of risk factors such as diabetes and/or
smoking, and the systemic impact of the periodontitis.

How might grading affect my treatment plan?
In the examples above, if a current smoker is assigned a Grade C, smoking
cessation would be incorporated into the treatment plan.
If the patient has diabetes mellitus, which is in moderate or poor control (HbA1c
> 7%) and a Grade C is assigned, the patient will be informed that his/her level of
diabetes control most likely has contributed to periodontitis.
In addition, if control is not improved, there is a risk for future progression of
periodontal disease.
This patient would be referred to his/her physician with a request to evaluate the
level of control and make adjustments for better control, if possible.
The treatment plan going forward will directly be influenced by patient
compliance. More intensive maintenance therapy may be recommended as part
of the treatment plan for both types of patient.

What is meant by the consensus statement, “a periodontitis patient is a
periodontitis patient for life”?
A patient who has periodontitis remains at risk for further periodontal
destruction even with treatment.
It is important to define a periodontitis patient as an “at-risk” individual because
this patient requires a more intensive level of maintenance and evaluation than a
patient who has not had periodontitis.
Thus, a periodontitis patient who has been treated and is now stable should not
return to a level of evaluation and maintenance identical to a patient who has
never had periodontitis (i.e., annual or semi-annual exam/prophylaxis).

How does this new disease construct impact what I submit for insurance? Will
third parties reimburse differently for a case if it is Stage II versus Stage III?
The AAP has met with several carriers to determine how the new classification
will affect them and, more specifically, how it will affect reimbursement. Across
the board, all have indicated that the classification will not affect reimbursement
at this time. Insurance companies do not reimburse based on severity of disease.
Third parties will still determine reimbursement based on the documentation
required for the treatment rendered (i.e., probing depths, radiographs showing
bone loss, etc.).
The classification will affect diagnosis codes; however, these are currently not
required for dental insurance reimbursement.
The AAP is working with the ICD-10 Coordination and Maintenance Committee
to adjust the ICD-10-CM diagnosis codes, and we are hopeful that changes will
be in place in 2020.

Future challenges in the classification of periodontal
diseases
As we enter the postgenomic era with our increased understanding of the bacteria
associated with periodontal infections and the genetic factors controlling host
responses to these infections, it would seem that a more mechanistic or etiological
classification could be devised.
It may eventually be possible to subclassify the multiple forms of ‘Chronic
Periodontitis’ into discrete microorganism/host genetic polymorphism groups such as:
Group A – Set .1 of microorganisms + Set .1 of genetic polymorphisms.
Group B – Set .2 of microorganisms + Set . 2 of genetic polymorphisms.
Group C – Set .3 of microorganisms + Set .3 of genetic polymorphisms.
Group D – Set .4 of microorganisms + Set .4 of genetic polymorphisms.

It will be necessary to address head on the nagging question, ‘When
are host-modifying factors (e.g. smoking, diabetes) so important that
they should be a principal part of the disease classification?’ That is,
in an evidence-based classification should there be a ‘smoking-
induced periodontitis’ or a ‘diabetic periodontitis?’ When do
modifying factors become an essential classification characteristic of
the disease?
Although tempting, terms based on assumed etiological or
pathogenic associations should be discouraged until there is a body of
data to support their use.

Genetic signature reveals new way to classify gum
disease
Currently, periodontal disease is classified as either "chronic" or "aggressive,"
based on clinical signs and symptoms, such as severity of gum swelling and
extent of bone loss.
"However, there is much overlap between the two classes," said study leader
Panos N. Papapanou. "Many patients with severe symptoms can be effectively
treated, while others with seemingly less severe infection may continue to lose
support around their teeth even after therapy. Basically, we don't know
whether a periodontal infection is truly aggressive until severe, irreversible
damage has occurred.“
A new system for classifying periodontal disease has been devised based on
the genetic signature of affected tissue, rather than on clinical signs and
symptoms. The new classification system, the first of its kind, may allow for
earlier detection and more individualized treatment of severe periodontitis,
before loss of teeth and supportive bone occurs.

By looking at the expression of
thousands of genes in gum tissue,
researchers can now classify most
cases of periodontitis into one of
two clusters. More severe cases of
the disease are represented under
the red bar, less severe cases
under the blue bar.

Conclusion
Why is classification of periodontal disease so difficult and so
controversial? The answer lies in the heterogeneity of the clinical
presentation and our lack of understanding of the true nature of
the differences between the different clinical presentations of
the disease.
We attempt to classify using evidence based upon the different
infections represented and on the host response. However, in
most cases our knowledge is incomplete or confused.
Much of the certitude that was felt in the 1980s that we had
reached a point where we could truly distinguish between the
different disease presentations in a scientific manner, has largely
evaporated.

It would seem that we are trying to classify diseases of which we
do not have sufficient knowledge. The present classification of
periodontitis looks surprisingly like a return to simplex and
complex.
Until we have greater understanding of the aetiology, the
bacteria associated with different periodontal infections and the
pathogenesis and genetics of periodontal diseases, it is
very likely that we will see further reclassifications at regular
intervals.

There are many unknowns and major challenges in the field of
periodontal diagnostics. We have no validated clinical, microbiologic,
biochemical, genetic, or host-response tests that predict who will and
who will not develop periodontitis.
In patients who have been treated for periodontitis and placed on a
maintenance program, we have no early warning system to identify
those who are on the verge of experiencing a recurrence of attachment
loss. In the future, we need to develop methods to: 1) identify a health-
associated host-microbe homeostasis in our patients and 2) detect
when disease-associated deviations in this homeostasis begin to
develop.
Solutions to these and other problems in periodontal diagnostics will
eventually be found. The solutions will, of course, come from scientific
advances in our understanding of the complex ecological interactions
between microorganisms and humans.

Biblography
 Classifying periodontal diseases - a long standing dilemma
Gary.C.Armitage. Perio2000 2002: vol 30; 9-23.
 Periodontal diagnosis in children and adolescents Introduction and
classification –Denis .F.Kinane ,Perio 2000 2001:vol 26;7-15
 Purpose & problems of periodontal disease classification- Ubele van der
velden, Perio 2000 2005:vol 39;13-21.
 Periodontics . Grant / Stern / Listergarten - 6th edition
Carranza’s clinical periodontology – 8th & 10th edition

Development of a classification system for periodontal diseases and conditions-
Gary.C.Armitage. Ann Perio: vol 4; 1999: 1-6.
The Periodontal Diseases Classification of the AAP –An Update .Colin.B.Wiebe et al.
J.Can.Dent Assoc.2000 vol66: 594-597.
 Understanding periodontitis in adolescents: Historical background Rodrigo López
International journal of dental clinics 2011:3(2):26-32

AAP Centennial Commentary: Theme 3 Evolution and Application of
Classification Systems for Periodontal Diseases — A Retrospective
Commentary - Gary C. Armitage
J of Periodontol 2014; vol 85, no. 3 : pg 369- 371
Genetic signature reveals new way to classify gum disease
March 21, 2014
Columbia University Medical Center
Panos N. Papapanou,
Science Daily
Gingival tissue transcriptomes identify distinct peridontitis phenotypes.
M. Kebschull et al. Journal of dental research 2014
 https://www.perio.org/2017wwdc
Periowiki.com holds copyright of this power point presentation only.
Patient case photographs, screen shots of tables credit – Google, textbooks and journal
articles (details mentioned in references section).

Classification of diseases and conditions affecting the periodontium

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