Classification of periodontal diseases /certified fixed orthodontic courses by Indian dental academy

INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education

www.indiandentalacademy.com

Classification systems
In the last 130 years, many classification system for
periodontal diseases have been used such as

Ramfjord and Ash 1979
Page and Schroeder 1982
Vogel and Cattabriga 1986
Suzuki 1988.
Grant, Stern, and Listgarten, 1988
European workshop on Periodontology 1993
World workshop in Clinical Periodontics 1989

Genco 1990
Ranney 1993

In 1989 classification system was developed that
included five types of periodontitis.
(i) Adult periodontitis
(ii) Early onset periodontitis
(iii) Periodontitis associated with systemic disease
(iv) Necrotizing ulcerative periodontitis
(v) Refractory periodontitis
The main drawbacks of this classification were
(i) Considerable overlap in disease categories
(ii) Absence of a gingival disease component
(iii) Inappropriate emphasis on age of onset of disease and
rates of progression
(iv) Inadequate or unclear classification criteria

The need to revise classification system for periodontal
diseases was emphasized during the 1996 World Workshop in
Periodontics. In 1997 the American academy of periodontology
responded to this and formed a committee to plan and organize an
international workshop to revise the classification system for
periodontal diseases.

On October 30 – November 2, 1999, the International
Workshop for a classification of Periodontal Diseases and conditions
was held and a new classification was agreed upon.


CHANGES IN THE CLASSIFICATION IN
PERIODONTAL DISEASES
 Addition of a section on “ Gingival Diseases”
 Replacement of “adult periodontitis” with “chronic
periodontitis”
 Replacement of “early onset periodontitis” with
“aggressive periodontitis”
 Elimination of a separate disease category for
“refractory periodontitis”

 Replacement of “necrotizing ulcerative periodontitis

with “Necrotizing periodontal diseases”

 Addition of a category on “Periodontal abscess”

 Addition of a category on “Periodontic endodontic

lesions”

 Addition of a category on “Development or acquired

deformities and conditions”

Classification of periodontal disease and condition (1999
international workshop for a classification of periodontal
disease and conditions)
The new classification (1999) is as follows:
1.GINGIVAL DISEASES
a) Dental plaque induced gingival disease.
(Can occur without attachment loss or on a periodontium with
attachment loss that is not progressing)
1.Gingivitis associated with dental plaque only:
a) Without other local contributing factors
b) With local contributing factors (See VIII A)

2.Gingival diseases modified by systemic factors
a) Associated with the endocrine system
1. Puberty assoicated gingivitis
2. Menstrual cycle associated gigivitis
3. Pregnancy assoicated
a) gingivitis
b) pyogenic granuloma
1. Diabetes mellitus assoicated gingivitis
c) assoicated with blood dyscrasias
1. leukemia assoicated gingivitis
2. Other
3. Gingival diseases modified by medications


d) drug influenced gingival diseases
1. drug influenced gingival enlargements
2. drug influenced gingivitis
a) oral contraceptive assoicated gingivitis
b) other
4.Gingival diseases modified by malnutrition
a) ascorbic acid deficiency gingivitis
b) other
B. Nonplaque induced Gingival lesions
1. Gingival disease of specific bacterial origin
a. Nesseria gonorrhea assoicated lesions
b. Treponema pallidum associated lesions
c. Streptococcal species assoicated lesions
d. Others
2. Gingival disease of viral origin
a) herpes virus infection
3. primary herpetic gingivostomatitis
4. recurrent oral herpes
5. www.indiandentalacademy.com
varicella zoster infections

b. other
1. Gingival disease of fungal origin
a) candida species infections
1. generalized gingival candidiasis
b. linear gingival erythema
c. histoplasmosis
d. other
4. Gingival lesions of genetic origin
a. hereditary gingival fibromatosis
b. other
5. Gingival manifestations of systemic conditions
a. mucocutaneous disorders
1. lichen planus
2. pemphigoid
3. pemphigus vulgaris
4. erythema multiforme
5) Lupus erythematosus
6) Drug-induced
7) Other www.indiandentalacademy.com

b. Allergic reactions
1) Dental restorative materials
a) Mercury
b) Nickel,
c) Acrylic
d) Other
2) Reactions attributable to
a) Toothpaste’s /dentifrice’s
b) Mouth rinses / mouth washes
c) Chewing gum additives
d) Foods and additives
3) Other

6) Traumatic lesions (factitious, iatrogenic,
accidental)

a) Chemical injury

b) Physical injury

c) Thermal injury

7) Foreign body reactions

8) Not otherwise specified (NOS)


II. Chronic Periodontitis
a) Localized
b) Generalized
III. Aggressive Periodontitis
a) Localized
b) Generalized
IV. Periodontitis as a manifestation of systemic diseases.
A) Associated with hematological. disorders.
1) Acquired neutropenia
2) Leukemias
3) Other

B) Associated with genetic disorders
1. Familial and cyclic Neutropenia
2. Down syndrome
3. Leukocyte adhesion deficiency syndromes
4. Papillon - Lefevre syndrome
5. Chediak – Higashi syndrome
6. Histiocytosis syndrome
7. Glycogen storage disease
8. Infantile genetic agranulocytosis
9. Cohen syndrome
10. Ehlers – Danlos syndrome (Types IV and VIII)
11. Hypophosphatasia
12. Other

V. Necrotising Periodontal Diseases
a) Necrotising ulcerative gingivitis
b) Necrotising ulcerative periodontitis
VI. Abscesses of the periodontium
a) Gingival abscess
b) Periodontal abscess
c) Periocoronal abscess
VII Periodontitis assoicated with endodontic lesions
A. Combined periodontal endodontic lesions
VIII. Developmental or Acquired Deformities and conditions
A. Localized tooth related factors that modify or predispose to plaque
induced gingival disease / periodontitis
1. Tooth anatomic factors
2. Dental restorations / appliances
3. Root fractures
4. Cervical root resorption and cemental tears

B. Mucogingival deformities and conditions around teeth
1. gingival / soft tissue recession
a. facial or lingual surfaces
b. interproximal (papillary)
2. lack of keratinized gingiva
3. decreased vestibular depth
4. aberrant frenum / muscle position
5. gingival excess
a. pseudopocket
b. inconsistent gingival margin
c. excessive gingival display
d. gingival enlargement (see section I, parts A3 and B4)
1abnormal color


C. Mucogingival deformities and conditions on edentulous
ridges
1. vertictal and / or horizontal ridge deficiency
2. lack of gingiva / keratinized tissue
3. gingiva / soft tissue enlargement
4. aberrant frenum / muscle position
5. decreased vestibular depth
6. abnormal color

D. Occlusal trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma

1. GINGIVAL DISEASES
Dental plaque induced gingival diseases
• Gingivitis that is associated with dental plaque
formation is the most common form of the gingival
disease.
• It has been proved that plaque induced gingivitis may
occurs on a periodontium with no attachment loss or
on a periodontium with previous attachment loss that
is stable and not progressing.


Gingivitis associated with dental plaque only

• Plaque induced gingival disease is the result of an
interaction between the microorganism found in the
dental plaque biofilm and the tissues and inflammatory
cell of host.
• The plaque host interaction can be altered by the
effects of local factors, systemic factors or both,
medications and malnutrition that can influence the
severity and duration of the response.

Gingival Diseases Modified by Systemic Factors
• Systemic factors contributing to gingivitis, such as
the endocrine changes associated with puberty,
menstrual cycle, pregnancy and diabetes may be
exacerbated because of the alterations in the gingival
inflammatory response to plaque.
• This is caused by the effects of the systemic
conditions on the cellular and immunological
functions of the host.
• These changes are most apparent during pregnancy,
when the prevalence and severity of gingival
inflammation may increase even in the presence of
low levels of plaque.

• Blood dyscrasias such as leukemia may alter immune
function by disturbing the normal balance of
immunologically competent white cells supplying
periodontium.
• Gingival enlargement and bleeding are common
findings and may be associated with, swollen, spongy
gingival tissues caused by excessive infiltration of
blood cells.


Gingival Diseases Modified by medications:
• Gingival diseases modified by medications are
increasingly prevalent because of the increased use of
anticonvulsant drugs, known to induce gingival
enlargement.
• Such as phenotoin, immunosuppressive drugs such as
cyclosporine A, and calcium channel blockers such as
nifedipine, verapamil, diltiazem and sodium
valproate.


• The development and severity of gingival
enlargement in response to medications is patient-
specific and may be influenced by uncontrolled
plaque accumulations.
• The increased use of oral contraceptives by pre-
menoposal woman has been associated with a higher
incidence of gingival inflammation and development
of gingival enlargement.


Gingival disease modified by Malnutrition
• Gingival disease modified by malnutrition may
have clinical descriptions of bright red, swollen and
bleeding gingiva associated with severe ascorbic
acid deficiency or scurvy.
• Nutritional deficiencies are known to affect immune
function a may have an impact on the hosts ability
to protect itself against some of the detrimental
effects of celluar products such as oxygen radicals.


Non – Plaque Incduced Gingival Lesions
Gingival Disease of Specific Bacterial Origin
• These disease are increasing in prevalance especially as a
result of sexually transmitted disease such as gonorrhea and
to a lesser degree syphillis.
• Oral lesions may be secondary to systemic infections or may
occur through direct infection.
• Streptococcal gingivitis or gingivo stomatitis is a rare
condition that may present as an acute condition with fever,
malaise and pain associated with acutely inflammed diffuse
red, and swollen gingiva with increased bleeding and
occasional gingival abscess formation.
• The gingival infections usually are preceded by tonsillitis
and have been associated with group A β hemolytic
steptococcal infections.

Gingival disease of Viral Origin
• It may be caused by a variety of
deoxyribonucleic acid (DNA) and ribonucleic
acid (RNA) viruses, the most common being
the herpes viruses.
• Lesions are frequently related to reactivation
of latent viruses especially as a result of
reduced immune function.


Gingival Disease of Fungal Origin
• It occurs most frequently on individuals who are
immunocompromised or in whom the normal oral
flora has been disturbed by long term use of broad
spectrum antibiotics.
• The most common oral fungal infection is candidiasis
caused by infection with candida albicans which also
can be seen under prosthetic devices the individuals
using topical steriods and in individuals with
decreased salivary flow increased salivary glucose, or
decreased salivary pH.


• A generalized candidal infection may manifest as
white patches on the gingiva, tongue or oral mucous
membrane than can be removed with a gauze leaving
a red, bleeding surface.
• In HIV infected individuals candidal infection may
present as erythema of attached gingiva and has
been referred to as linear gingival erythema or HIV
associated gingivitis.


Gingival Disease of Genetic Origin
• One of the most clinically evident conditions is
hereditary gingival fibromatosis that exhibits
autosomal dominant or (rarely) autosomal recessive
modes of inheritance.
• The gingival enlargement may completely cover the
teeth, delay eruption and present as an isolated
finding or be associated with several more
generalized syndromes.


Gingival Manifestations of Systemic Conditions
• It may appear as desqumative lesions, ulceration
of gingiva or both.
• Allergic reactions that manifest with gingival
changes are uncommon but have been observed
in association with several restorative materials,
tooth pastes, mouth washes, chewing gum and
foods.


Traumatic Lesions

Traumatic lesions may be factitial (produced by artifical
means; unintentionally produced) as in the case of tooth brush
trauma resulting in gingival ulceration, recession or both;
iatrogenic (trauma to the gingiva induced by the dentist or
health professional) as in the case of preventive or restorative
care that may lead to traumatic injury of the gingiva; or
accidental as in the case of damage to the gingiva through
minor burns from hot food and drinks.


Foreign Body Reactions

• Foreign body reactions lead to localized
inflammatory conditions of the gingiva and are
caused by the introduction of foreign material into
the gingival connective tissues through breaks in
epithelium
• Eg. Introduction of amalgam into gingiva during
the placement of restoration or an extraction of a
tooth leaving an amalgam tatoo or the introduction
of abrasives during polishing procedures.

CHRONIC PERIODONTITIS
It is a common plaque induced periodontal infection that is
major cause of tooth loss throughout the world.
Its important clinical features are
• Most prevalent in adults but can occur in children and adolescents.
• Amount of destruction is consistent with the presence of local
factors.
• Associated with a variable microbial pattern
• Slow to moderate rate of progression but may have periods of
rapid progression.
• Can be associated with local predisposing factors.
• May be modified by or associated with systemic disease
• Can be modified by or factors other than systemic disease such as
cigarette smoking and emotional stress.

AGGRESSIVE PERIODONTITIS
• Aggressive periodontitis is much less common than chronic
periodontitis and affects a narrower range of younger patients.

• It occurs in localized and generalized forms and the two forms
differ in many respects with regard to their etiology and
pathogenesis.

• LAP and GAP were once called localized and generalized juvenile
periodontitis respectively.

• However these terms were replaced with LAP and GAP
terminology because they do not depend on questionable age
based classification criteria.

Both forms of aggressive periodontitis share the

following common features.
• Expect for the presence of periodontitis patients

are otherwise clinically healthy
• Rapid attachment loss and bone destruction

• Familial aggregation


Some of the important secondary features of both forms of
aggressive periodontitis are
• Amount of microbial deposits are inconsistent with the severity
of periodontal tissue destruction.
• Increased proportions of Actinobacillus actino –
mycetemcomitans and in some populations, Porphyromonas
gingivalis may increased.
• Phagocyte abnormalities

• Hyper responsive macrophage phenotype, including increased
levels of prostaglandin E2 and inter leukin – 1 β
• Progression of attachment loss and bone loss may be self
arresting

Specific features of localized and generalized
aggressive periodontitis.
Localized Aggressive Periodontitis
• Circum Pubertal onset
• Robust serum antibody to infecting agents
• Localized first molar / incisor presentation with
interproximal attachment loss on at least two
permanent teeth one of which is a first molar and
involving no more than two teeth other than first
molars and incisors.


Generalized Aggressive Periodontitis

• Usually affecting individuals less than 30 years but
patients may be older
• Poor serum antibody response to infecting agents
• Pronounced episodic nature of the destruction of
attachment and alveolar bone
• Generalized interproximal attachment loss affecting
at least three permanent teeth other than first
molars and incisors.


Periodontitis as a manifestation of systemic diseases
There are two general catogories of systemic
disease that have periodontitis as a frequent
manifestation

1. Certain hematologic disorders (eg acquired
neutropenia, leukemia) and
2. Some genetic disease (eg. Familial / cyclic
neutropenia, down syndrome, leucocyte adhesion
deficiency syndromes, papillon lefevre syndrome).


NECROTIZING PERIODONTAL DISEASE
• Necrotizing periodontal infections include
necrotizing ulcerative gingivtis (NUG) and
necrotizing ulcerative periodontitis (NUP).
• In both the condition there is a rapid onset
of pain associated with development of
necrotic and ulcerative lesions of marginal
gingiva, particularly involving
interproximal sites.

NECROTIZING ULCERATIVE GINGIVITIS
The two most significant criteria used for the diagnosis
of NUG are
1. Presence of interproximal necrosis and ulceration
2. A histroy of rapid onset of gingival soreness and pain.
• The interproximal necrosis and ulceration take the form of
eroded crater like depressions of one or more interproximal
gingival papillae sometimes referred to as having “ Punched
Out” appearance.
• Marked halitosis is present in most patients with NUG.
• Some patients have a pseudomembrane covering the
ulcerated areas of the gingiva.

It is a heterogenous film composed of fibrin, bacteria,
sloughed epithelial cells and other debris. It can be easily
removed or wiped of by frictional forces of eating and is
therefore frequently absent. NUG are occasionally associated
with lymphadenopathy, increased salivation, fever, malavise
and anorexia.

Predisposing factors for NUG in adult patients from
North America and Europe include.

1. Emotional stress
2. Heavy cigarette somking
3. Lack of sleep
4. Poor dietary habits
5. Immunosuppression.

• In children from underdeveloped countries, NUG appears
to be associated with malnutrition or the debilitating and
immunosuppressive effects of viral or parasitic infection.
• The common features of all the predisposing factors of
NUG is that they decrease host resistance to periodontal
infections.
• In every immunosuppressed children, NUG is believed to
be the first stage of noma or cancrum oris, a severe necrotic
infection that caused massive destruction of the tissues of
the oral cavity and the face.


Necrotizing Ulcerative Periodontitis
• Compared to NUG, NUP always involves
considerable loss of periodontal attachment and
alveolar bone.
• The term necrotizing ulcerative periodontitis did not
appear in classification systems for periodontal
disease until the later 1980s at the peak of the AIDS
epidemic.
• It was added to the classification systems primarily
because of the increasing appearance of a rapidly
destructive and intensely painful form of
periodontitiswww.indiandentalacademy.com
in HIV infected patients.

• In some patients with NUP there were exposure and
sequestration of alveolar bone.
• Severe immuno suppression from other sources such
as cancer chemotherapy and advanced protein
energy malnutrition also can lead to the
development of NUP.


ABSCESSES OF PERIODONTIUM
An abscess is a circumscribed collection of pus.

Factors that predispose to abscess formation are

1. Deep periodontal pockets.
2. Incomplete removal of sublingival calculus during
scaling and root planing
3. Occlusion of the pocket orifice by foreign bodies
4. Administration of antibiotics to patients with
periodontitis in the absence of mechanical therapy


Periodontitis Associated with Endodontic Leisions
• Infections of periapical tissues caused by the pulpal
death (i.e endodontic lesions) can often locally join
with separate infections emenating from periodontal
pockets.

• This coalescence of endodontic and periodontal
infections has termed combined periodontal–
endodontic lesions.

Developmental or Acquired Deformities and Conditions
• There are many developmental or acquired deformities and

conditions of periodontal tissues that technically are not

disease.

• They are included in most classifications of periodonatl disease

because they may be important modifiers of susceptibility to

periodontal infections or can dramatically influence treatment

outcomes.


Localized tooth related factors that modify or
predispose to plaque induced periodontal
diseases.
• Tooth related factors that can be associated with
an increased risk for development of plaque
induced periodontal disease include, cervical
enamel projections, enamel pearls, furcation
anatomy, tooth position, root proximity and
anamalous grooves in roots.
• Defect in dental restorations such as poor
contours and marginal discrepancies can increase
the risk of periodontal infections.

Mucogingival Deformities and conditions around Teeth

Mucogingival deformities refer to a group of congenital,
developmental, or acquired defects in the normal relation between
keratinized gingival tissues and nonkeratinized alveolar mucous. These
deformities are

1. Gingival/soft tissue recession
- Facial or lingual surfaces
- Inter proximal (papillary)
2. Lack of keratinzed gingiva
3. Decreased vestibular depth
4. Aberrant frenum/muscle position
5. Gingival excess
- Pseuodpockets
- Inconsistent gingival margin
- Excessive gingival display
- Gingival enlargement
6. Abnormal colourwww.indiandentalacademy.com

Mucogingival Deformities and Conditions on
Edentulous Ridges.
There are:
• Vertical and/or horizontal ridge deficiency
• Lack of gingival /keratinized tissue
• Gingival / soft tissue enlargement
• Aberrant frenum /muscle position
• Decreased vestibular depth
• Abnormal color.

Occlusal Trauma:
Damage to periodontal tissues can occur during a
variety of conditions involving occlusal loads and
forces that exceed the capacity of the periodontium to
with stand them
eg: Primary occlusal trauma
Secondary occlusal trauma


Classification of periodontal diseases /certified fixed orthodontic courses by Indian dental academy

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