CLASSIFICATION OF PERIODONTAL

DISEASES

PRESENTED BY,

SWETHA SATHEESKUMAR FIRST YEAR POST GRADUATE DEPARTMENT OF

PERIODONTICS

1
CONTENT

1. INTRODUCTION
2. DEFINITION
3. USES OF CLASSIFICATION
4. NEED FOR CLASSIFICATION
5. HISTORICAL DEVELOPMENT OF CLASSIFICATIONS SYSTEM
6. CLINICAL CHARACTERISTICS PARADIGM [1870 -1920] 7.
CLASSICAL PATHOLOGY PARADIGM [1920 – 1970]
 8. INFECTION /HOST RESPONSE PARADIGM
9. CURRENT CLASSIFICATION SYSTEMS OF PERIODONTAL DISEASES
10. CHANGES IN THE CLASSIFICATION FOR PERIODONTAL DISEASES
11. FUTURE CHALLENGES IN THE CLASSIFICATION OF PERIODONTAL
DISEASES
12. CONCLUSION
13. REFERENCES

2
INTRODUCTION

Understanding of the etiology and pathogenesis of oral disease and conditions is continually
changing with increased scientific knowledge.The initial classification systems were based on
the clinical features of the diseases (1870-1920).Then came the concept of classical pathology
(1920-1970).Presently – concepts of infectious etiology of periodontal diseases and host
response (1970).Most important landmark – current understanding of periodontal diseases
was the work done by Loe et al (1986) on natural history of periodontal diseases, and
observed that progression of periodontal diseases naturally without interfering.

Diagnosis is defined as the act of identifying a disease from its signs and symptoms, whereas
classification is defined as the act or method of distribution into groups. Here we are dealing
with the periodontal condition which is clinically characterized by three symptoms: loss of
connective tissue attachment, loss of alveolar bone support, and inflamed pathological
pockets.
On the basis of these three symptoms one diagnostic name for this condition would be
appropriate, e.g. destructive periodontal disease. However, if age, distribution of lesions,
degree of gingival inflammation, putative rate of breakdown, response to therapy, etc., are
also taken into account, numerous diagnostic names are needed. In order to be able to
communicate about patients, clinicians have always felt the need for diagnostic names and
classifications for these diseases, preferably on the basis of putative etiologic factors. At
present, controversies about definitions of diseases continues, not only in the periodontal field
but also in medicine.

Our understanding of the etiology and pathogenesis of oral diseases and 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, it any, clarification
by scientific laboratory testing.

DEFINITION

• ‘‘Systematic arrangements in groups or categories according to established criteria’’

(Merriam-Webster 2010)

3
NEED FOR CLASSIFICATION

• It provides us with a framework to come to a diagnosis.

• The intricacy of periodontal diseases can be understood by classifying various diseases. •
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 • To
obtain more knowledge about the causation of periodontal diseases •
Formulate treatment plan and predict the outcome of treatment
• To understand the etiology, pathology of the diseases of the periodontium. •
Facts can be filled for future references.
• Helps to communicate among clinicians, researchers, educators, students, epidemiologists
and public health workers.
The term periodontal disease has referred for some time to all diseases which affect one
or more tissues from the periodontium. Age has always been an important parameter in
periodontal diagnosis.

HISTORICAL DEVELOPMENT OF CLASSIFICATION SYSTEMS Classification of

periodontal diseases can be placed into three dominant paradigms .They are 1. Clinical

characteristics paradigm

2. Classical pathology paradigm

3. Infection /host response paradigm

[j perio 2000 ,lyons H kerr DM Hine MK ]

4
CLINICAL CHARACTERISTICS PARADIGM [1870 -1920]

Very little was known about the etiology and pathogenesis of periodontal diseases back then.
Accordingly, the diseases were classified almost entirely on the basis of their clinical
characteristics supplemented by unsubstantiated theories about their cause. At the time, one of
the main debates about the nature of periodontal diseases was whether they were caused by
local or systemic factors. Most authors considered these diseases to be primarily caused by
local factors whereas some believed that systemic disturbances played a dominant etiological
role. Many of the advocates for the etiological role of local factors also acknowledged that in
some cases both local and systemic factors were important.

In the late 1800s and early 1900s clinicians used case descriptions and their personal
interpretation of what they saw clinically as the primary basis for classifying periodontal
diseases. Their opinions survive in the literature in the form of written abstracts or summaries
of the proceedings of these meetings. Indeed, John M. Riggs(1811–1875), an American dentist
who lectured so widely on the treatment of periodontal diseases that periodontitis was called
‘Riggs’ disease’ by many of his colleagues, rarely published any papers on the subject. Riggs’
thoughts and opinions were most often summarized by others

Formal papers on the classification of periodontal diseases were rare in the late 1800s and
early 1900s. Typical publications on the subject usually represented the opinion of a single
person who almost always based the classification on clinical observations and theoretical
explanations of causation.

C .G. DAVIS IN 1879 – three distinct forms of destructive periodontal disease

1 . Gingival recession with minimal or no inflammation

This was due to ‘... feeble vascular action ...’ and trauma from tooth brushing or other
sources

2. Periodontal destruction secondary to lime deposits

‘The gum retires slowly ... and the alveolar border, deprived of nutrition at the point of
pressure, is consentaneously absorbed.’ Davis apparently believed that calculus
exerted mechanical pressure on the gingiva causing the alveolar bone to resorb
because of lack of nutrition

5
3. Riggs disease the hallmark of which was loss of alveolus without loss of gum

The perceived problem was a ‘necrosed alveolus’ or death of the periodontal

membrane. ‘... we get a disease that is initiated and continued without any visible
mechanical irritant in many cases; and I believe the death of the peridental membrane,
depriving the alveolus of nutrition, accounts for the death and disintegration of the
bone; or, as is believed by some, among them Dr Waters, of Boston, the alveolus is
destroyed by vegetable parasites’.

G .V BLACK CLASSIFICATION OF PERIODONTAL DISEASES IN 1886

1. Constitutional gingivitis
 It including mercurial gingivitis, potassium iodide gingivitis and scurvy

2. a painful form of gingivitis

Now termed necrotising ulcerative gingivitis [NUG] but he never used the term 3.

Simple gingivitis

This was associated with the accumulation of debris that eventually led to calcic
inflammation of the peridental membrane.

4. calcic inflammation of periodontal membrane

This was associated with salivary or serumal calculus. There was generalised pattern
of destruction of alveolar bone. The destruction usually occurred slowly. Now this is
known as chronic periodontitis

5. phagedenic pericementitis [phagedenic = spreading ulcer or necrosis ]

This condition shared many features with ‘calcic inflammation of the peridental
membrane’ but there was an irregular pattern of destruction and not much dental
calculus. Destruction of the alveolar bone can occur slowly or rapidly. In a later
publication, Black replaced the term ‘phagedenic pericementitis’ with ‘chronic
suppurative pericementitis’.

6
Demerits

• Little or no scientific evidence was used to support the opinions of the clinicians of
the time.

• No generally accepted terminology or classification system for periodontal diseases

was adopted during this era.

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. What emerged
from this was that there were at least two forms of destructive periodontal disease
inflammatory and non inflammatory [degenerative or dystrophic]. It was primarily based on
the over interpretation of histopathological studies from a group of Viennese investigators led
by gottlieb and orbans.

Gottlieb 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 [ie cementopathia].This
cemental defect was presumably initiated by the degeneration of the principal fibres 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 that
some young patients with relatively clean mouths had massive and localized bone loss with
only minimal or no overt signs of gingival inflammation.

GOTTLIEB CLASSIFICATION 1928

Inflammatory – schmutz pyorrhoea [result of the accumulation of deposits on the

teeth and characterized by inflammation, shallow pockets and resorption of the
alveolar bone]

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Degenerative or atrophic –
1. diffuse alveolar atrophy
2. paradental pyorrhoea
3. occlusal trauma

DEMERITS

• No microbial analysis.

• Inflammatory process is over interpretated as degenerative process. •

Gingival diseases not included.

ORBAN 1942 [classical pathology paradigm ]

Inflammation

1. Gingivitis [little or no pocket formation ;it can include ulcerative form – vincents ]

A. Local [calculus,food impaction,irritating restorations,drug action etc]

B. Systemic
- Pregnancy
- Diabetes
- Other endocrine dysfunctions
-Tuberculosis
-Syphilis
-Nutritional disturbances
- Drug action
-Allergy
-Hereditary
- Idiopathic etc
2. Periodontitis

A. Simplex [secondary to gingivitis ]- bone loss,pockets,abscesses can form;

cases have calculus

8
B. Complex [secondary to periodontosis ] –etiologic factors similar to
periodontitis ;cases have little ,if any calculus .

Degeneration

I. Periodontosis [as a rule attacks young girls and older men ;often caries immunity]

A. Systemic disturbances

- Diabetes

- Endocrine dysfunctions

- Blood dyscrasias
 - Nutritional disturbances

- Nervous disorders

- Infectious diseases [acute & chronic]

B. Hereditary

C. Idiopathic

Atrophy

I. Periodontal atrophy [recession ,no inflammation, no pockets ,osteoporosis ]

A. Local trauma [eg. From toothbrush

B. Presenile
C. Senile
D. Disuse
E. Following inflammation
F. Idiopathic

9
Hypertrophy

I. Gingival hypertrophy

- Chronic irritation

- Drug action [eg. Dilantin sodium]

- Idiopathic [eg.gingivoma, elephantiasis, fibromatosis]

Traumatism

I. Periodontal traumatism

A. Occlusal trauma
 [Periodontology 2000 vol 30 ;2002 .9- 23] DEMERITS

• Conclusion that some forms of periodontal diseases were caused by non inflammatory or
degenerative process was primarily based on over interpretation of histopathological
studies.

• No scientific basis for retaining the concept that there were non – inflammatory or
degenerative forms of destructive periodontal diseases.

• No convincing evidence that Gottlieb’s hypothesis [degenerative nature] was right.

WHO CLASSIFICATION -1961

WHO expert committee on the dental health in 1961 suggested that etiology plays secondary
and accessory part in classification . Clinical assessment lacks sufficient precision to serve as
a foundation for classification. The most valid basis for classification is therefore one based
on general pathology.

Gingivitis can be acute or chronic

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MERITS

Periodontitis can be acute or chronic

acute

periodontal abscess
chronic

ulcerative periodontitis simplex [it is charaterized by bone loss,pocket,abscess

formation,and calculus deposits]
complex [irregular bone loss ]

• Acute and chronic conditions are easily identified

DEMERITS

• Degenerative and neoplastic processes are left out

• Considered only inflammatory periodontal diseases.

• Not considered periodontal traumatism

• Systemic diseases not included .

McPHEE AND COWLEY CLASSIFICATION -1966

GINGIVITIS

A. Acute Gingivitis
a. Acute specific - ulceromembrane gingivitis , herpectic gingivitis,coccal gingivitis

b. Acute non specific

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B. Chronic Gingivitis
a. Chronic non specific – chronic edematous gingivitis
b. Chronic hyperplastic gingivitis
c. Chronic atrophic gingivitis

PERIODONTITIS

A. Acute Non Specific

Periodontal abscess

B. Chronic Non Specific

1. periodontitis simplex[horizontal bone loss]
2. periodontal complex [ vertical bone loss]
 MERITS

• Based entirely on inflammation

• Simplified – considered both specific and non specific inflammatory changes • Also

considered host responses .in small percentage of cases ,lab procedures may defines
an alteration in host responses ,which may be a factor or the presence of infection
predominantly by over particular group of organism.

DEMERITS
Not stated about periodontal traumatism

INFECTION /HOST RESPONSE PARADIGM 1970

ROBERT KOCH 1876

He provided experimental proof of the germ theory of disease
W.D .MILLER 1890
Three factors are to be taken into consideration in every case of pyorrhoea alveolaris. 1 .

predisposing circumstances

2. local irritation

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3 . Bacteria

PRICHARD 1972

Inflammation surface destruction

- NUG
- Herpetic gingivostomatitis
- Desquamative gingivitis
- Oral ulcers

Diseases affecting the surfaces or gingival

-inflammation without destruction

- marginal gingivitis

- generalised diffuse gingivitis

-gingival enlargement

Diseases affecting deeper structures

-chronic destructive periodontal diseases

-periodontal abscess

- periodontal traumatism

-primary traumatism

-secondary traumatism

MERITS

• Considered the rate of tissue destruction

• Considered topography , morphology,etiology and pathology

DEMERITS

• Rate of bone destruction is considered ie slow or rapid process •

Not included systemic modifiers of periodontal diseases

13
PAGE AND SCHROEDER [ 1982]

• Prepubertal periodontitis

1. Generalised
2. Localized

• Juvenile periodontitis

• Rapidly progressing periodontitis

• Adult type periodontitis

MERITS

1. Simplified , convenient and uncomplicated

2. Systemic and local factors that modify the host response to bacteria and their products
included
3. Designed to accommodate additional forms of diseases as new insights are gained and
additional forms are identified
DEMERITS
1. Gingival diseases not included
2. Non –validated age dependent criteria
3. Periodontal endodontic lesions not included
4. Occlusal trauma not included

AMERICAN ACADEMY OF PERIODONTOLOGY – 1986

I Juvenile periodontits

A Prepubertal periodontitis

B Localized juvenile periodontitis

C Generalized juvenile periodontitis

II Adult periodontis

III Necrotizing ulcerative gingivo-periodontitis

IV Refractory periodontitis.

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TOPIC’S CLASSIFICATION – 1986

ACUTE CONDITIONS

1. Gingivitis

a) Specific – ulceromembranous, herpetic, coccal gingivitis

b) Non-specific

2. Periodontitis

a) Periodontal abscess

b) Pericoronitis

CHRONIC CONDITIONS

1. Gingivitis

a) Plaque- associated

b) Symptomatic

2. Periodontitis

a) Simplex (adults)

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b) Complex
- Generalized forms

Rapidly progressive: type A

Rapidly progressive: type B

Prepubertal

- Localized forms

Juvenile, Post-juvenile, Prepubertal

c) Symptomatic

3. Recession

MERITS

– Acute stages & chronic stages are well differentiated.

– Considered modifiers of periodontal diseases in the category of chronic conditions.

DEMERITS

• Nothing is stated about the occlusal trauma.

• Periodontal- endodontic lesions are not considered.

• Age of affected patients is considered in classifying periodontal diseases (similar to

Suzuki’s classification).

WEATHERFORD CLASSIFICATION -1987

DISEASES AFFECTING THE SURFACE OF GINGIVA

A. Inflammation without destruction.

Marginal gingivitis

Generalized diffuse gingivitis

16
Gingival enlargement
 B. Inflammation with Surface Destruction

- NUG

- Herpetic gingivostomatitis

- Desquamative gingivitis

- Oral ulcers

DISEASES AFFECTING THE DEEPER STRUCTURES

A. Early onset periodontitis

Prepubertal – localised /

generalized

Juvenile periodontitis

Rapidly progressing periodontitis

Post-pubertal periodontitis

Adult type, Rapidly progressing type

B. PERIODONTAL TRAUMATISM

Primary traumatism

Secondary traumatism

C. PERIODONTAL ABSCESS

MERITS

• Clearly differentiates gingivitis, gingival enlargement, NUG, periodontitis & so on. •

Useful in teaching

17
DEMERITS
 • Age-dependent criteria.
• Rate of bone destruction

JOHNSON ET AL.1988

I Childhood periodontitis including specific syndromes such as Papillon-Lefevre

II Juvenile periodontitis: localized; generalized

III Post-juvenile periodontitis

IV Adult onset periodontitis: slowly progressive; rapidly progressive

V Periodontitis associated with systemic diseases such as diabetes, scurvy,

immunodeficiencies (including AIDS), immunosuppressive states, blood dyscrasias

VI Traumatic periodontitis, e.g. gingival recession and loss of attachment as a result of

abrasion during oral hygiene practice (toothbrushing, wood sticks, charcoal, brick dust;
trauma from occlusion)

VII Iatrogenic periodontitis, due to inappropriate restorations or inappropriate instrumentation

of the gingival crevice.

GRANT ,STERN AND LISTGARTEN [1988]

• Bacterially induced diseases

-Gingivitis

-Periodontitis
- Adult type
- Postjuvenile
- Early onset
- Juvenile

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 - Localized
- Generalised
a) Acute necrotizing ulcerative gingivitis
b) Acute abscess
c) Pericoronitis

• Functionally induced diseases

Traumatic occlusion
Disuse atrophy

• Trauma

Habits ,accidents

MERITS
• May be useful in differential diagnosis.
• Gingival hyperplasia could be fitted into various categories.

DEMERITS
• Age-dependent criteria in diagnosing diseases.
• Rate of progression is considered.

SUZUKI [1988]

➢ GINGIVITIS

• Plaque associated gingivitis

• ANUG

• Steroid hormone influenced gingivitis

• Medication induced gingival overgrowth

• Other forms of gingivitis

➢ PERIODONTITIS
 • Adult periodontitis

19
• Rapidly progressing periodontitis
o Type A
o Type B
• Juvenile periodontitis
• Postjuvenile periodontitis
• Prepubertal periodontitis

MERITS
• Age of the patient
• Rate of bone destruction is considered.
• Rapidly progressing periodontitis is again subclassified . i.e RPP type A and
RPP type B
DEMERITS
• Non-validated age-dependent criteria.
• Not considered periodontal abscess
• Not considered periodontal – endodontal lesions.
• Occlusal trauma not included.

World Workshop in Clinical Periodontics (1988)

Gingivitis

• Childhood gingivitis

• Chronic (adult) gingivitis

• Acute necrotizing ulcerative gingivitis

Periodontitis

• Adult Periodontitis:

Possible sub-groups:

– High risk

– Normal risk
 20
– Refractory periodontitis

• Early Onset Periodontitis:

– Localized juvenile periodontitis

– Rapidly progressive periodontitis

– Pre-pubertal periodontitis

* Localized

* Generalized

– Periodontitis associated with systemic diseases

World Workshop in Clinical Periodontics (1989)

I. Adult periodontitis.

II. Early onset periodontitis.

•Prepubertal

– Generalized or localized

• Juvenile

– Generalized or localized

• Rapidly progressive periodontitis

III. Periodontitis associated with systemic diseases

• Down’s Syndrome

• Diabetes – Type I

• Papillon – Lefévre syndrome

• AIDS and other diseases

IV. Necrotizing ulcerative periodontitis

 21
V. Refractory periodontitis

• This classification was proposed by Page and Schroeder in 1982.

• Main features;

This classification was based on the infection/ host response paradigm depended heavily on

✓ the age of the affected patients (Prepubertal and Juvenile

periodontitis),

✓ rate of progression (Adult and Early periodontitis),

✓ host factors (Periodontitis associated with systemic disease) and

✓ response to the conventional therapy (Refractory periodontitis)

Drawbacks associated with 1989 AAP classification:

i. It does not include gingivitis/gingival disease category.

ii. Periodontitis categories had nonvalidated age dependent criteria.

iii. There was extensive crossover in rates of progression of the different categories of
periodontitis. Rapidly progressive periodontitis was a heterogeneous category.

iv. There was extensive overlap in the clinical characteristics of the different categories of
periodontitis.

v. Refractory periodontitis was a heterogeneous category.

vi. Prepubertal periodontitis was a heterogeneous category.

vii. Finally, different forms of periodontitis proposed in the classification shared many
microbiologic and host response features, which suggested extensive overlap and
heterogeneity among the categories.

Genco (1990)

• Periodontitis in adults.

• Periodontitis in juveniles

– Localized form
 22
– Generalized form

• Periodontitis with systemic involvement

– Primary neutrophil disorders

– Secondary or associated neutrophil impairment.

– Other systemic diseases

• Miscellaneous conditions

Ranney (1993)

Gingivitis

• Gingivitis, plaque bacterial

• Non-aggravated

• Systemically-aggravated by sex hormones, drugs, systemic

diseases. • Necrotizing ulcerative gingivitis

• Systemic determinants unknown

• Related to HIV

• Gingivitis, non-plaque

• Associated with skin diseases, allergic, infections.

Periodontitis

• Adult periodontitis

– Non-aggravated

– Systematically-aggravated (neutropenias, leukemias, lazy leukocyte syndrome, AIDS,

diabetes mellitus, Crohn’s disease, Addison’s disease).

• Early onset periodontitis:

 23
– Localized early onset periodontitis

– Neutrophil abnormality

– Generalized early onset periodontitis, neutrophil abnormality, immunodeficient. •

Early onset periodontitis related to systemic disease

– Leukocyte adhesion deficiency, hypophosphatasia , Papillon- Lefevre syndrome ,

neutropenias , leukemias, Chediak- Higashi syndrome, AIDS, diabetes mellitus type-I,
trisomy-21, histiocytosis X, Ehlers Danlos syndrome (type VIII)

• Early onset periodontitis, systemic determinants unknown

• Necrotizing ulcerative periodontitis

– Systemic determinants unknown

– Related to HIV

– Related to nutrition

• Periodontal abscess

[Periodontology 2000, Vol. 2. 1993, 13-25] 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.

European Workshop on Periodontology (1993)

• Adult periodontitis

Begins at the 4th decade of life, slow rate of progression of disease.

• Early onset periodontitis

24
th
Begins before the 4 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.

All the above-mentioned classification systems have been widely used by clinicians and
research scientists throughout the world, unfortunately they have been many shortcomings
including:

1. Considerable overlap in disease categories.

2. Absence of a gingival disease component

3. Inappropriate emphasis on age of onset of disease and rates of progression.

4. Inadequate or unclear classification criteria.

Hence, the need for a revised classification system for periodontal diseases was emphasized
and in 1999, the international workshop had considered designing a new classification system.

CURRENT CLASSIFICATION SYSTEMS OF PERIODONTAL DISEASES

25
 INTERNATIONAL WORKSHOP FOR THE CLASSIFICATION OF
THE PERIODONTAL DISEASES BY THE AMERICAN ACADEMY
OF PERIODONTOLOGY (AAP) 1999

CLASSIFICATION OF PERIODONTAL DISEASES AND CONDITIONS

Gingival Diseases

Plaque-induced gingival diseases

Non plaque-induced gingival lesions

Chronic Periodontitis

Localized

Generalized

Aggressive Periodontitis

Localized

Generalized

Periodontitis as a Manifestation of Systemic Diseases

Necrotizing Periodontal Diseases

Necrotizing ulcerative gingivitis (NUG)

Necrotizing ulcerative periodontitis (NUP)

Abscesses of the Periodontium

Gingival abscess

Periodontal abscess

Pericoronal abscess

Periodontitis Associated with Endodontic Lesions

26
Endodontic-periodontal lesion

Periodontal–endodontic lesion

Combined lesion

Developmental or Acquired Deformities and Conditions

✓ Localized tooth-related factors that predispose to plaque-induced

gingival diseases or periodontitis

✓ Mucogingival deformities andconditions around teeth.

✓ Mucogingival deformities and conditions on edentulous ridges.

✓ Occlusal trauma.

[carranza’s 11th edition] GINGIVAL DISEASES

Dental Plaque–Induced Gingival Diseases

These diseases may occur on a periodontium with no attachment loss or on a periodontium

with attachment loss that is stable and not progressing.

I. GINGIVITIS ASSOCIATED WITH DENTAL PLAQUE ONLY

A. Without local contributing factors

B. With local contributing factors

II. GINGIVAL DISEASES MODIFIED BY SYSTEMIC FACTORS.

A. Associated with endocrine system

1. Puberty-associated gingivitis

2. Menstrual cycle associated gingivitis

3. Pregnancy associated

a. Gingivitis

b. Pyogenic granuloma
 27
4. Diabetes mellitus associated gingivitis B.

Associated with blood dyscrasias

1. Leukemia-associated gingivitis

2. Other

III. GINGIVAL DISEASES MODIFIED BY MEDICATIONS

A. Drug-influenced gingival diseases

1. Drug-influenced gingival enlargements

2. Drug-influenced gingivitis

a.Oralcontraceptive–associatedgingivitis

b. Other

IV. GINGIVAL DISEASES MODIFIED BY MALNUTRITION

A . Ascorbic acid deficiency gingivitis

B. Other

Non–Plaque-Induced Gingival Lesions

I. Gingival diseases of specific bacterial origin

A. Neisseria gonorrhoeae

B. Treponema pallidum

C. Streptococcus species

D. Other

II. Gingival diseases of viral origin

A. Herpes virus infections

1. Primary herpetic gingivostomatitis

 28
2. Recurrent oral herpes

3. Varicella zoster

B. Other

III. Gingival diseases of fungal origin

A. Candida species infections: generalized gingival candidiasis B. Linear

gingival erythema

C. Histoplasmosis

D. Other

IV. Gingival lesions of genetic origin

A. Hereditary gingival fibromatosis

B. Other

V. Gingival manifestations of systemic conditions

A. Mucocutaneous lesions

1. Lichen planus

2. Pemphigoid

3. Pemphigus vulgaris

4. Erythema multiforme

5. Lupus erythematosus

6. Drug induced

7. Other

B. Allergic reactions

1. Dental restorative materials

a. Mercury
 29
b. Nickel

c. Acrylic

d. Other

2. Reactions attributable to:

a. Toothpastes or dentifrices

b. Mouth rinses or mouthwashes

c. Chewing gum additives

d. Foods and additives

3. Other

VI. Traumatic lesions (factitious, iatrogenic, or accidental)

A. Chemical injury

B. Physical injury

C. Thermal injury

VII. Foreign body reactions

VIII. Not otherwise specified

[carranza’s 11th edition]

1 .GINGIVITIS 2. (a) hormonal effects of pregnancy. (b) and (c) By medications. (b)
antihypertensive drug, nifedipine, (c) By cyclosporine,
 30

AMERICAN ACADEMY OF PERIODONTOLOGY (1999) CLASSIFICATION

I. Gingival diseases

A. Gingival diseases caused by plaque

1. Gingivitis exclusively caused by plaque

a. With no local modifying factors

b. With local modifying factors

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2. Gingival diseases modified with systemic factors
a. associated with endocrine system

1) Gingivitis connected with puberty

2) Gingivitis connected with the menstrual cycle

3) Connected with pregnancy

a) Gingivitis in pregnancy

b) Pyogenic granuloma

4) Gingivitis connected with diabetes mellitus

b. Connected with blood disease

1) Gingivitis connected with leukaemia

2) Other diseases

3. Gingival diseases modified by application of medications

a. Gingival diseases caused by medications

1) Gingival growths caused by medications

2) Gingivitis caused by medications

a) Gingivitis connected with oral contraceptives

b) Other medications

4. Gingival diseases caused by malnutrition

a. Gingivitis due to lack of vitamin C

b. Others

32
B. Gingival lesions not induced by plaque
 1. Gingival diseases of specific bacterial etiology a.

Lesions connected with Neisseria gonorrhoeae b.

Lesions connected with Treponemapallidum c. Lesions

connected with streptococci

d. Others

2. Gingival diseases of viral etiology

a. Infection with the Herpes virus
1) Primary herpetic gingivostomatitis
2) Recurring oral herpes
3) Varicella zoster infection

b. Others

3. Gingival diseases of fungal etiology

a. Infection with candida

1) Generalised gingival candidiasis
b. Linear gingival erythema
c. Histoplasmosis
d. Others

4. Gingival diseases of genetic etiology

a. Inherited fibromatosis of the gingiva

b. Others

5. Systemic diseases which manifest on the gingiva

33
a. Changed mucous membrane
1) Lichen planus
 2) Pemphigoid
3) Pemphigus vulgaris
4) Erythema multiformis
5) Lupus erythematosus
6) caused by medications
7) Others
b. Allergic reactions
1) Material in restorative dentistry
a) Mercury
b) Nickel
c) Acrylic
d) Others
2) Reaction to:
a) Toothpaste
b) Mouthwashes
c) Additives in chewing gum
d) Nutritive substitutes
3) Others

6. Traumatic lesions (iatrogenic, accidents)

a. Chemical
b. Physical
c. Thermal

7. Reaction to foreign bodies

8. Not otherwise defined

II. Chronic periodontitis (CP)

A. Localised
B. Generalised

34
III. Aggressive periodontitis (AP)

A. Localised
 B. Generalised

IV. Periodontitis as a manifestation of systemic diseases (NP)

A. Connected with blood diseases

1. Acquired neutropenia

2. Leukaemia

3. Others

B. Connected with genetic disorders

1. Family or cyclic neutropenia

2. Down’s syndrome

3. Leucocyte adhesive deficiency syndrome

4. Papillon-Lefevre syndrome

5. Chediak-Higashi syndrome

6. Histiocytosis or Eosinophilic granuloma syndrome

7. Glycogen storage syndrome

8. Infantile genetic agranulocytosis

9. Cohen’s syndrome

10. Ehlers-Danlos syndrome, type IV and VIII AD

11. Hypophosphatasia

12. Others

C. Not otherwise defined

35
V. Necrotizing periodontal diseases

A. Necrotizing ulcerous gingivitis /NUG

B. Necrotizing ulcerous periodontitis (NUP)

VI. Periodontal abscesses

A. Gingival abscess

B. Periodontal abscess

C. Pericoronal abscess

VII. Periodontitis with endodontal lesions

A. Combined perio-endo lesion

VIII. Developmental and acquired deformation and conditions

A. Localised dental factors which encourage plaque, caused by gingivitis / periodontitis 1.

Anatomy of the teeth

2. Reconstruction of teeth/effect of the device

3. Fractured root

4. Resorption of roots and (cement pearls)

B. Mucogingival deformities and relations in the tooth vicinity

1. Recession

a. Facially and orally

b. Approximally

2. Lack of gingival keratinization

3. Shortened gingival attachment

4. Localisation of the tongue or lip frenum

5. Gingival enlargement

36
a. Pseudo-pockets

b. Irregular development of the gingival edge

c. Excessive gingival presentation

Main features of AAP 1999 classification system are:

i. Comprehensive section of gingival diseases is included in this classification. ii. There is

replacement of the term adult periodontitis with chronic periodontitis, since epidemiological
evidence suggests that chronic periodontitis may also be seen in adolescents.
iii. There is elimination of separate categories of rapidly progressive periodontitis and
refractory periodontitis because of the lack of evidence that they represent separate
conditions.
iv. There is replacement of the term early onset periodontitis with aggressive periodontitis
largely because of the clinical difficulties in determining the age of onset in many
of these cases. The author of this new classification also questions the use of the
term juvenile periodontitis for the same reasons. They have replaced the term with
localized and generalized aggressive periodontitis. The term aggressive was added
because bone and tissue destruction occurs rapidly as compared with other
periodontitis.
v. A new classification group of periodontitis as a manifestation of systemic disease has
been created and this includes those cases of prepubertal periodontitis directly
resulting from known systemic diseases.
vi. There are also new group categories of abscesses of the periodontium, periodontic –
endodontic lesions and developmental/acquired deformities/conditions.

PERIODONTITIS

Periodontitis is defined as “an inflammatory disease of the support- ing tissues of the teeth
caused by specific microorganisms or groups of specific microorganisms, resulting in
progressive destruction of the periodontal ligament and alveolar bone with increased probing
depth formation, recession, or both.”

37
Classification of the Various Forms of Periodontitis

AAP World Workshop in Clinical Periodontics, 1989

• Adult periodontitis

- Age of onset greater than 35yr

- Slow rate of disease progression
- No defects in host defences
 • Early onset periodontitis[may be prepubertal,juvenile,or rapidly
progressive]
- age of onset less than 35yr
- rapid rate of disease progression --Defects in host defences
- Associated with specific microflora

• Periodontitis associated with systemic disease

-Systemic diseases that predispose to rapid rates of periodontitis

-Diseases: diabetes, Down syndrome, HIV infection, Papillon-Lefèvre
syndrome

• Necrotizing ulcerative periodontitis -Similar to acute necrotizing ulcerative

gingivitis but with associated clinical attachment loss
-

• Refractory periodontitis

- Recurrent periodontitis that does not respond to treatment

European Workshop in Periodontology, [1993]

• Adult periodontitis

-Age of onset: fourth decade of life

-Slow rate of disease progression

-No defects in host response

38
• Early-onset periodontitis

- Age of onset: before fourth decade of life

- Rapid rate of disease progression --Defects in host defense

• Necrotizing periodontitis
 - Tissue necrosis with attachment and bone loss

DEMERITS

• Lacked necessary for adequate categorization of the broad spectrum of periodontal

diseases encountered in clinical practice.

• Gingival diseases not included.

AAP International Workshop for Classification of Periodontal Diseases,[ 1999]

• Chronic periodontitis

• Aggressive periodontitis

• Periodontitis as a manifestation of systemic diseases

Chronic Periodontitis

Chronic periodontitis in the 1999 classification has replaced the term adult periodontitis.

The following characteristics are common to patients with chronic periodontitis: •

Prevalent in adults but can occur in children.

• Amount of destruction consistent with local factors.

• Associated with a variable microbial pattern.

• Subgingival calculus frequently found.

• Slow-to-moderate rate of progression with possible periods of rapid progression.

39
• It is associated with the following:

1. Systemic diseases such as diabetes mellitus and human immunodeficiency virus

 (HIV) infection.

2. Local factors predisposing to periodontitis.

3. Environmental factors such as cigarette smoking and emotional

stress.

CLASSIFICATIONS

slight - 1 to 2mm clinical attachment loss

moderate - 3 to 4 mm clinical attachment loss

severe - more than 5mm clinical attachment loss

TREATMENT

1. Plaque control
2. scaling and root planing
3. correction of local plaque retentive factors
4. antimicrobial chemotherapy
5. periodontal surgery
6. supportive periodontal therapy

40
CHRONIC PERIODONTITIS

Aggressive Periodontitis

Aggressive periodontitis replaces the category ‘early onset periodontitis’ which in the 1989
AAP and 1993 European classification embraced a number of diseases affecting young
patients.

The following characteristics are common in patients with aggressive periodontitis:

• Otherwise clinically healthy patient.

• Rapid attachment loss and bone destruction.

• Amount of microbial deposits inconsistent with disease severity. •

Familial aggregation of diseased individuals.

The following characteristics are common but not universal:

• Diseased sites infected with Actinobacillus actinomycetemcomitans

. • Abnormalities in phagocyte function.

• Hyperresponsive macrophages, producing increased prostaglandin E2 (PGE2) and

interleukin-1β (IL-1β).

• In some cases, self-arresting disease progression.

41
Aggressive periodontitis may be further classified into localized and generalized forms

localised form • Circumpubertal onset of disease. • Localized first

molar or incisor disease with proximal attachment TREATMENT
loss on at least two permanent teeth, one of which generalised form
is a first molar. • Robust serum antibody response
to infecting agents.

• Usually affecting persons under 30 years of age

(however, may be older).
• Generalized proximal attachment loss affecting
at least three teeth other than first molars and
incisors.
• Pronounced episodic nature of periodontal
destruction
•Poor serum antibody response to infecting
agents

1. Specific, antimicrobial therapy periodontitis based on microbial

analysis 2. smoking cessation

3. debridement

4. possible periodontal surgery

5. supportive periodontal therapy

Periodontitis as a Manifestation of Systemic Diseases

Periodontitis may be observed as a manifestation of the following systemic diseases:

1. Hematologic disorders

a. Acquired neutropenia

b. Leukemias

c. Other

42
2. Genetic disorders

a. Familial and cyclic neutropenia

b. Down syndrome

c. Leukocyte adhesion deficiency syndromes

d. Papillon-Lefèvre syndrome

e. Chédiak-Higashi syndrome

f. Histiocytosis syndromes

g. Glycogen storage disease

h. Infantile genetic agranulocytosis

i. Cohen syndrome

j. Ehlers-Danlos syndrome (types IV and VIII autosomal dominant [AD]) k.

Hypophosphatasia

l. Other

3. Not otherwise specified

Causes

Associated with disorders of blood or blood forming organs such as neutropenia, leukemia ,
or genetic disorders

Signs and symptoms

Generalized and localized forms of severe destruction of bone and connective tissue tooth
support

Treatment

Treatment of systemic disease: atraumatic plaque control, antimicrobial rinses , supportive

periodontal therapy

43
 C

yclic neutropenia down syndrome

ABSCESSES OF THE PERIODONTIUM

According to Meng (1999) abscesses are classified into:

(a) Gingival abscesses

(b) Periodontal abscesses

(c) Pericoronal abscesses

GINGIVAL ABSCESSES

• Gingival abscess is a localized painful, rapidly expanding lesion usually of sudden

onset.

• It is generally limited to the marginal gingiva or interdental papilla. •

Etiology:
(i) Irritation from foreign substances,
toothbrush bristle

44
(ii) Apple core
(iii) Lobster shell forcefully embedded into the gingiva.
PERIODONTAL ABSCESSES

Depending on the cause of acute infectious process, two types of periodontal abscess occur:

A. Periodontitis-related abscesses:

(a) Exacerbation of chronic lesion

(b) Post-therapy periodontal abscesses

(i) Post-scaling periodontal abscesses

(ii) Post-surgery periodontal abscesses

(iii) Postantibiotic periodontal abscesses

B. Non-periodontitis-related abscesses:

(a) Impaction of foreign body in the gingival sulcus or periodontal

pocket. (b) Root morphology alterations or iatrogenic endodontic

perforations. History: periodontal treatment

Periodontal diseases

Clinical findings

1. Vital pulp responses

2. Periodontal disease evident

3. Periodontal probing release pus

45
4. Swelling is generalized and located around the involved tooth and gingival margin. Seldom
with a fistulous tract

5. Pain is usually dull, constant and less severe than in a periapical abscess. Pain is localized
and patient usually can locate the offending tooth

Radiographic findings

1. Alveolar crest bone loss

2. Angular bone defect
3. Furcation involvement findings

Response to treatment

1.Respond dramatically to release of pus .

2.Subgingival debridement.

46
PERICORONAL ABSCESSES
History 1. Caries, fracture, toothwear
2. Restorative and endodontic treatment
Clinical findings

1. Questionable/non responsive pulp tests

2. Narrow probing defect (May be isolated lesion)
3. Advanced caries, advanced toothwear, large restoration, discolored tooth 4.
Swelling is localized often with fistulous opening in the apical area 5. Pain is
usually severe, throbbing and patient may not be able to locate the offending
tooth.

Radiographic findings

1. Apical radiolucency
2. Endodontic or post perforations

Response to treatment
1. Responds poorly, or not at all to periodontal treatment

NECROTIZING PERIODONTAL DISEASE

Two forms of necrotizing periodontal disease

• Necrotizing ulcerative gingivitis (NUG)

• Necrotizing ulcerative periodontitis (NUP)

• NUG has been previously classified under “gingival diseases” or “gingivitis” because
clinical attachment loss is not a consistent feature

• NUP has been classified as a form of “periodontitis” because attachment loss is present •

Recent reviews of the etiologic and clinical characteristics of NUG and NUP have suggested
that the two diseases represent clinical manifestations of the same disease, except that distinct
features of NUP are clinical attachment and bone loss.

47
• As a result, both NUG and NUP have been determined as a separate group of •

diseases that have tissue necrosis as a primary clinical feature

Necrotizing ulcerative gingivitis (NUG)

➢ Acute, painful disease confined to gingiva

➢ Symptoms are

-abrupt onset of pain

-necrosis of the tip of the interdental papilla

-Ulcer formation with white-yellowish or gray pseudomembranes,demarcated by

linear erythema

-halitosis

-regional lymphadenitis and subfebrile condition may occur

-Peak incidence in patients in their 20s

➢ Etiology

-invasive gram negative, obligate anaerobes

Spirochetes
Fusobacteria
Prevotella intermedia
- Presumed association with herpesviruses
Eg. Human cytomegalovirus

➢ Risk factors

-poor oral hygiene

- cigarette smoking
-psychological stress ,lack of sleep
-HIV infection

➢ Histopathology

-nonspecific ,acute necrotizing inflammation

-ulcerated areas are covered by pseudomembranes consisting of a network of

48
fibrin ,perished epithelial cells ,leukocytes ,erythrocytes and bacteria -connective
 tissue beneath contains widened and proliferating vessels and a dense infiltrate of
neutrophilic granulocytes, plasma cells ,and macrophages , invasive fusobacteria
and spirochetes

Necrotizing ulcerative periodontitis (NUP)

• Acute periodontal infection characterized by an expansion of necrotic lesions into the

periodontal ligament and alveolar bone usually occurs as a manifestation of severe
weakness of the immune system [immune suppression ,nutritional deficit]

• Rapid attachement loss ,often without formation of deep pocket Sockets ,but with the
possibility of bony sequestration

• Closely associated with HIV infection/AIDS .

PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESION

Periodontal–Endodontic Lesions

• In periodontal–endodontic lesions, bacterial infection from a periodontal pocket

associated with loss of attachment and root exposure may spread through
accessory canals to the pulp, resulting in pulpal necrosis.

• In the case of advanced periodontal disease, the infection may reach the pulp
through the apical foramen.

• Scaling and root planing removes cementum and underlying dentin and may lead to
chronic pulpitis through bacterial penetration of dentinal tubules.
 49
• periodontitis-affected teeth have been scaled and root planed with no evidence of
pulpal involvement.

Endodontic–Periodontal Lesions

• In endodontic–periodontal lesions, pulpal necrosis precedes periodontal changes. • A

periapical lesion originating in pulpal infection and necrosis may drain to the oral
cavity through the periodontal ligament, resulting in destruction of the periodontal
ligament and adjacent alveolar bone.

• This may present clinically as a localized, deep, periodontal probing depth extending
to the apex of the tooth .

• A resultant extensive alveolar ridge defect may necessitate reconstructive surgery

before placement of implants and prosthesis to reestablish a functional and esthetic
outcome.

• Pulpal infection also may drain through accessory canals, especially in the area of
the furcation, and may lead to furcal involvement through loss of clinical
attachment and alveolar bone.

combined periodontic endodontic lesions

➢ Close endodontic periodontic interrelationship exits

_via apical foramen

-via lateral and furcal foramina
-via dentinal tubules after removal of root cementum

➢ Infections may spread from one area into other ;

- Retrograde pulpitis ,if and when the plaque front within a periodontal pocket
reaches the apex or accessory pulp channels
- Spread of an endodontic [periapical] infection into the periodontal ligament .

DEVELOPMENTAL/ACQUIRED DEFORMITIES AND CONDITIONS

Developmental or acquired deformities and conditions

✓ Localized tooth related factors that modify or predispose to plaque induced gingival
diseases or periodontitis

50
1. Tooth anatomic factors

2. Dental restorations or appliances

3. Root fractures

4. Cervical root resorption and

cemental tears

✓ Mucogingival deformities and conditions around teeth

1. Gingival or soft tissue recession

A. Facial or lingual surfaces
B. Interproximal (papillary)
2. Lack of keratinized gingiva
3. Decreased vestibular depth
4. Aberrant frenum or muscle position
5. Gingival excess
A. Pseudopocket
B. Inconsistent gingival margin
C. Excessive gingival display
D. Gingival enlargement
E. Abnormal color

✓ Mucogingival deformities and conditions on edentulous edges

I. Vertical and or horizontal ridge deficiency
II. Lack of gingiva or keratinized tissue
III. Gingival or soft tissue enlargements
IV. Aberrant frenum or muscle position
V. Decreased vestibular depth
VI. Abnormal color

✓ Occlusal trauma
1. Primary occlusal trauma

2. Secondary occlusal trauma

51
OCCLUSAL TRAUMA

Excessive occlusal forces do not lead to plaque associated periodontal diseases and attachment
loss,but they may accelerate the progression of already existing periodontitis.

-Primary occlusal trauma - periodontal injury due to excessive occlusal forces in a normal
tooth supporting apparatus [normal bone and attachment level]

-secondary occlusal trauma – periodontal injury due to normal or excessive forces in a

reduced periodontium [loss of bone and attachment]

CHANGES MADE IN THE CLASSSIFICATION

Addition of a section on gingival diseases

• The 1989 classification did not include a section on gingival diseases and lesions

• An important feature of the section on dental plaque induced diseases is

acknowledgment that clinical expression of gingivitis can substantially modified by
systemic factors, medications and malnutrition

• The section on dental non-plaque induced diseases includes a wide range of disorders
that affect the gingiva

Replacement of “adult periodontitis” with “chronic periodontitis”

• Epidemiological data and clinical experience suggest that the form of periodontitis
found in adults can also be seen in adolescents

• The age dependent nature of adult periodontitis designation created problems

• It was more accurate to adopt a non-specific term such as chronic periodontitis to

characterize this constellation of destructive periodontal diseases

• It is did not imply that this diseases was non-responsive to this treatment.
• Also it was concludes that rate of progression should not be used to exclude people from
receiving the diagnosis of chronic periodontitis.

Replacement of “Early-onset Periodontitis” with Aggressive periodontitis

52
• there is considerable uncertainty about arbitrarily setting an upper age limit for patients
with so called early onset periodontitis therefore it was decided to discard
classification terminologies that were age dependent or required knowledge of rate of
progression.

• RPP designation has been discarded and the patients are assigned to either generalized
aggressive periodontitis or chronic periodontitis categories

• most of the patients who have been given the diagnosis of generalized prepubertal
periodontitis actually had one of the varieties of systemic conditions that interfere with
resistance to bacterial infections

• therefore such patients should be placed under the heading of periodontitis as

manifestation of systemic diseases.

• prepubescent children who have periodontal destruction without any modifying

systemic conditions would, depending on a variety of secondary features fit under the
category of chronic periodontitis or aggressive periodontitis

Elimination of separate disease category for Refractory periodontitis

▪ There is a diversity of clinical conditions and treatments under which periodontal

therapy fails to arrest the progression of periodontitis

▪ Refractory periodontitis was not a single disease entity, therefore it was concluded that
it could be applied to all forms of periodontitis

Clarification of the designation “Periodontitis as a manifestation of Systemic

Diseases

• category has been retained since it is clear that destructive periodontal disease can be
manifestation of certain systemic diseases

• Diabetes mellitus and cigarette smoking are not included as they are significant
modifiers of all forms of periodontitis
 Replacement of “Necrotizing ulcerative periodontitis” with “Necrotizing
periodontal diseases”

• Both NUG and NUP might be manifestation of certain systemic diseases such as HIV,
and then it was more appropriate to place them under manifestation of systemic
diseases

53
• The reason that this was not done was there are many factors other than systemic
diseases that appear to predispose to development of NUG and NUP such as
emotional stress and cigarette smoking

Addition of a category on “Periodontal abscess

• Periodontal abscess are a part of periodontitis and formation of a separate disease

category is not justified

• Since periodontal abscess present special diagnostic and treatment challenges, they
deserve to be classified apart from other periodontal diseases

Addition of a category on “Developmental or Acquired Deformities and

Conditions”

• These are not separate diseases; they are important modifiers of the susceptibility to
periodontal diseases or can dramatically influence outcomes of treatment.

CLASSIFICATION BY VAN DER VELDEN (2000)

classification was based on four dimensions, i.e. extent, severity, age, and clinical
characteristics.

Classification based on the extent of the disease:

If teeth are missing, the class description should still reflect the clinical image of the patient.
Therefore it was decided for cases with£14 teeth to omit the class semi-generalized and to
change the number of teeth for the generalized class to 8–14
 Permanent ⁄ mixed n<14 Primary dentition
dentition No. of
teeth present n>14

Incidental 1 tooth 1 tooth 1 tooth

Localized 2- 7 tooth 2-7 tooth 2-4 tooth

Semi-generalized 8- 13 teeth - 5 – 9 teeth

Generalized >14 teeth 8–14 teeth >10 teeth

54
Classification based on severity of disease per tooth. The fact that either attachment lossor
bone loss can be used for the classification of severity implies that although it may be
important to know the actual root length in a given patient radiographs are not a prerequisite
for the classification of severity.

Classification based on age:

Early onset periodontitis

Prepubertal periodontitis <12 years

Juvenile periodontitis 13–20 years

Postadolescent periodontitis 21–35 years

Adult periodontitis >36 years

If in patients classified as adult periodontitis it can be demonstrated on the basis of

documentation that they already had moderate or severe periodontitis before the age of 36
years, the disease is classified as early onset periodontitis

Classification based on the severity of disease per tooth

Minor bone loss <1 ⁄3 of the root length
or attachment loss <3 mm

Moderate bone loss > 1 ⁄3 and <1 ⁄2 of the

root length or attachment loss 4–5
mm

Severe bone loss >1 ⁄2 of the root length

 or attachment loss ‡ 6 mm

Classification based on the severity of disease per tooth. The mean estimated root length
based on the literature is approximately 12 mm; in the case of incidental disease, the severity
category at that particular tooth is mentioned

The classification is ascertained in the following way:

• First, the severity category is determined for each tooth;

55
• Next, the extent category is determined by counting the number of teeth with the most
severe condition;
• Diagnosis on the basis of clinical characteristics is added if
applicable; • Diagnosis on the basis of age.

Classification based on clinical characteristics:

Necrotizing periodontitis interdental gingival necrosis,
bleeding and pain

Rapidly progressive periodontitis documented rapid breakdown (at any

age), i.e. rapidly progressive
periodontitis patients showing a
progression of ‡ 1 mm interproximal
attachment ⁄ bone loss per year at
affected sites

Refractory periodontitis documented, no or minimal pocket

depth reduction at single rooted teeth
after proper initial therapy and ⁄or
further attachment loss despite the
proper execution of various treatment
modalities
Periodontitis associated with systemic diseases, i.e. periodontitis in subjects suffering from
general diseases, or periodontitis in subjects using medication, which enhance the rate and
severity of periodontal breakdown is not identified as a specific class of periodontitis.
However, the association with such a condition should be added to the diagnosis.

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

56
these infections ,it would seem that a more mechanistic or etiological classification could
be devised.

✓ One of the main problems associated with any attempt at subclassifying this or other forms
of periodontitis ,is that these infections are polymicrobial and polygenic.

✓ The clinical expression of these diseases is altered by important environmental and host
modifying conditions

✓ 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 micro organism + set # 1of genetic polymorphisms •

Group B –set #2 of micro organism + set # 2 of genetic polymorphisms •

Group C –set # 3 of micro organism + set # 3 of genetic polymorphisms •

Group D –set # 4 of micro organism + set # 4 of genetic polymorphisms

It is necessary to superimpose on these microorganism / host genetic polymorphisms
groupings the effect of environmental or host-modification factors i.e. “Smoking-induced
Periodontitis” or “Diabetic Periodontitis”

57
CONCLUSION

Classification systems for periodontal diseases have evolved based on the

understanding of the nature of these diseases at the time the classifications were
proposed. Revisions to existing systems have been largely influenced by three
dominant paradigms that reflect thinking at the time the classifications were proposed.
Although classification systems for periodontal diseases currently in use are firmly
based on and dominated by the Infection/ Host Response paradigm, some features of
the older paradigms are still valid and have been retained. Since it is probable that
essentially all dentists and periodontists in the world are convinced that most
periodontal diseases are infections, it is unlikely that the Infection/Host Response
paradigm will be replaced in the near future.
Before a classification firmly based on the etiological and pathogenic characteristics of
periodontal infections can be devised, numerous fundamental breakthroughs will have
to occur in our understanding of host–microbial interactions and the environmental
factors that affect them. New classification systems appear complex and too
comprehensive at a glance. However, some of the former classifications which looked
much straightforward were frequently unsuitable and confusing to use. The new
classification of periodontal diseases has made application in practice possible. Neither
 is this classification ideal. However, it is the first time that a group of internationally
acknowledged experts have produced a generally accepted and scientifically founded
classification of periodontal diseases.

58
REFERENCES

➢ NEWMAN carranza’s 11 th edition

➢ Essentials of Clinical Periodontology and Periodontics 3 rd edition SHANTIPRIYA

➢ Periodontics revisited SHALU BATHLA First edition

➢ Contemporary periodontics: Genco, Goldman & Cohen

➢ Annals of periodontology. 1999, vol-1

➢ Periodontal diagnosis and classification of periodontal diseases. Gary C.

Armitage.Perio 2000;34:9-21

➢ Classifying periodontal diseases – A long standing dilemma. Gary C. Armitage. Perio

2000. 2002; 30: 9-23

➢ Purpose and problems of periodontal disease classification. Perio 2000. 2005; 39: 132

➢ Diagnosis and classification of periodontal disease. J Highfield Australian Dental

Journal 2009; 54:(1 Suppl): S11–S26

➢ Development and Evolution of Classification of Periodontal Diseases: An Insight. Dr.

Mahajan Aaditi, Dr. Kolte Rajashri, Dr. Kolte Abhay. International dental journal of
student’s research; 2015;3(1)

➢ Pini-Prato G. The Miller classification of gingival recession: limits and drawbacks. J

Clin Periodontol 2011; 38: 243–245.

➢ The Periodontal Disease Classification System of the American Academy of

Periodontology —An Update J Can Dent Assoc 2000; 66:594-7

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