By: Sarah Kahil

Course: PERIO511

7/1/2016

NEW CLASSIFICATION OF
PERIODONTAL DISEASE
I. Gingival Diseases:
Dental plaque induced gingival diseases
Non-plaque induced gingival diseases
II. Chronic Periodontitis (Localized/Generalized)
III. Aggressive Periodontitis (Localized/Generalized)
IV. Periodontitis as a manifestation of systemic diseases.
Associated with hematologic disorders
Associated with genetic disorders
Not otherwise specified (NOS)
V. Necrotizing Periodontal Diseases
a) Necrotizing Ulcerative Gingivitis (NUG)
b) Necrotizing Ulcerative Periodontitis (NUP)
VI. Abscesses of the Periodontium
a) Gingival abscess
b) Periodontal abscess
c) Pericoronal abscess
VII. Periodontitis Associated + Endodontic Lesions
a) Endodontic periodontal lesion
b) Periodontal endodontic lesion
c) Combined lesion
VIII. Developmental or Acquired deformities & conditions
a) Localized tooth related factors that predispose to plaque
induced gingival diseases or periodontitis.
- Tooth anatomic factor
- dental
restoration/appliance

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By: Sarah Kahil

Course: PERIO511

7/1/2016

- Root fracture
resorption/ C tears

- cervical root

b) Mucogingival deformities or conditions around teeth:

- Gingival recession
- Lack of keratinized gingiva
- Decreased vestibular depth
- Aberrant frenum
- Gingival enlargement
c) Mucogingival deformities and conditions on edentulous ridges:
- Vertical and horizontal ridge deformities
- Lack of gingiva/ keratinized tissue
- Gingival soft tissue enlargement
- Aberrant frenum
- Decreased vestibular depth
- Abnormal color
CHANGES IN CLASSIFICATION SYSTEM FOR PERIODONTAL
DISEASES (1999)
I. Addition of gingival diseases
II. Replacement of adult periodontitis with chronic periodontitis
III. Replacement of EOP with aggressive periodontitis
IV. Elimination of refractory periodontitis
V. Clarification of periodontitis as manifestation of systemic diseases
VI. Replacement of NUP with Necrotizing periodontal diseases
VII. Addition of periodontal abscess
VIII. Addition of periodontic endodontic lesions
IX. Addition of developmental or acquired deformities and conditions
So, the term chronic periodontitis was used because:

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By: Sarah Kahil

Course: PERIO511

7/1/2016

- Less restrictive
- No age dependent
- No rate of progression dependent
Classification of chronic Periodontitis is according to:
Extent
(Nr. of sites involved)
1. Localized = < 30%
2. Generalized > 30%

Severity
(Amount of CAL)
- Slight 1-2 mm
- Moderate 3-4 mm
- Severe > 5 mm

N.B: Recurrent Periodontitis represents a return of periodontitis and it

is not a separate disease.
N.B: rapidly progressive periodontitis (1889) is discarded, WHY?
Because it depends on the progression rate and requires at least
2 consecutive ex. At a long period without treatment intervention,
this is difficult in routine clinical practice.
III. Replacement of early onset Periodontitis with Aggressive
Periodontitis
The term E.O.P (1889) was used as a collective designation of
dissimilar periodontal destruction that affect young patients (early
onset).
E>O>P were renamed using the term aggressive periodontitis.
N.B: patients who meet the clinical criteria for:
LJPlocalized aggressive periodontitis
GJP..Generalized aggressive periodontitis
So the term Early Onset Periodontitis is discarded and replaced by the
term Aggressive Periodontitis which is either:
- Localized
Generalized

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By: Sarah Kahil

Course: PERIO511

7/1/2016

The common features of localized and generalized forms of

aggressive periodontitis are:
1. Except for the presence of periodontitis, patients are clinically
healthy.
2. Rapid attachment loss and bone destruction
3. Familial aggression
4. Secondary features are generally but NOT universally present:
i) Amount of microbial deposits are inconsistent with the severity
of periodontal destruction.
ii) Elevated levels of A.A and P.G, in some populations
iii)Phagocytic abnormality
iv)Elevated levels of PGE2 and IL 1B
v) Progression of AL and bone loss may be self-arresting

I. Gingival Diseases
1. Dental plaque induced gingival diseases
A) Gingivitis with D.P only without/with local contributing factors
B) Modified by Systemic Factors:
a. Endocrine system
- Puberty
- Menstrual cycle
- Pregnancy
- Diabetes mellitus
b. Blood dyscrasias
e.g. leukemia associated gingivitis
C) Modified by medications:
a. Drug influenced gingival enlargement
b. Drug influenced gingivitis (oral contraceptive)
D) Modified by Malnutrition
- Ascorbic acid deficiency
- other
2. Non-plaque induced Gingival Lesions
a) Bacterial origin
b) Viral origin
c) Fungal origin
d) Genetic origin (hereditary gingival fibromatosis)
e) Gingival manifestations of systemic conditions

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By: Sarah Kahil

Course: PERIO511

7/1/2016

- Mucocutaneous
- Allergic reactions : dental restorative material (Hg, Acrylic),
reaction to (tooth paste, mouth wash, food)
f) Traumatic lesions (chemical, physical, thermal)
g) Foreign body reactions
h) Not otherwise specified (NOS)

CHRONIC PERIODONTITIS

Most common type

Slowly progressive disease
Attachment and alveolar bone loss
Cardinal symptoms pocket formation and/or recession and
gingival inflammation
Systemic or environmental factors modify host response to plaque
accumulation (diabetes, smoking, stress) progression more
aggressive.
Occurs at any age
Major Clinical and Etiological Characteristics
a) Microbial formation: Porphyromonas gingivalis, Tannerella
forsythia, Fusobacterium nucleatum, campylobacter recta,
Elkenella corrodens, Prevotella intermedia, spirochete species
b) Periodontal inflammation
c) Progressive attachment loss and alveolar bone loss
PORPHYROMONAS GINGIVALIS
-

Black pigmented
Anaerobic
Gram ve
Site of colonization gingival sulcus
Pathogenesis of chronic periodontitis
P. gingivalis cytotoxic metabolic end products, have low molecular
easily penetrate periodontal tissue and interrupt the host cell
activity.

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By: Sarah Kahil

Course: PERIO511

7/1/2016

TANNERELLA FORSYNTHESIS
- When colonizes in periodontally healthy sites, it converts diseased
sites.

N.B: the presence of continued bleeding on probing at subsequent

visits is indicator of presence of:
Inflammation
Attachment loss progresses continuously or in episodic bursts
of disease activity.
(Severity) on amount of CAL:

Attachment
loss
Furcation
involvement
Mobility
Bone loss

MILD
1-2 mm

MODERATE
3-4 mm

SEVERE
5 or >

minimal

moderate

Severe T-T

Little
minimal

Slight/moderate excessive
horizontal
horizontal/angul
ar
++
+++

Plaque/calculu +
s
Bleeding
+

+/exudate

+/exudate

Clinical Features:
a) Supragingival and subgingival plaque accumulation
b) Gingival inflammation and pocket formation
c) Increase crevicular fluid and suppuration
d) Gingival bleeding spontaneous upon slight provocation
e) Loss of attachment and alveolar bone
f) Vertical and horizontal bone loss
g) Tooth mobility

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By: Sarah Kahil

Course: PERIO511

7/1/2016

Radiographically:
Bone loss (horizontal or vertical)
Disease Distribution
- Site specific disease
- Clinical signs due to direct site specific effects of subgingival
plaque
- One tooth surface, other surfaces (normal A.L.)
Extent (Nr. of sites involved)
- Localized Periodontitis: when <30% sites affected
- Generalized Periodontitis: as > 30% of sites affected
Pattern of bone loss:
Horizontal: when A.L. and bones loss proceed at uniform rate.
Associated + Suprabony pockets
Vertical: when attachment and bone loss on tooth > than on
adjacent surface associated + angular bony and Infrabony pocket
formation
Disease Severity:
Mild: periodontal destruction not more than 1-2 mm CAL
Moderate: periodontal destruction not more 3-4 CAL
Severe destruction not more 5 mm or > CAL
Symptoms:
Usually painless
Sensitivity to hot, cold or both
Areas of localized dull pain sometimes radiate deep into jaw
Areas of food impaction
Gingival tenderness and itching
Prevalence:
Increased in age
Females and males

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By: Sarah Kahil

Course: PERIO511

7/1/2016

Not all cases respond to therapy, so referred to as refractory

periodontitis.
AGGRESSIVE PERIODONTITIS
A rapidly progressive form characterized by early age of clinical
manifestations.
Difference between aggressive and chronic periodontitis:
1. Age of patient
2. Rapid attachment loss and alveolar bone loss in otherwise healthy
patients.
3. Familial aggregations in most cases
4. Nature of composition of subgingival bacterial flora
5. Amount of microbial plaque is inconsistent with periodontal
destruction
6. Elevated numbers and in some proportions of A.
actinomycetemcomitans (and/or P. gingivalis in some populations)
in subgingival plaque
7. Phagocytic abnormalities
8. Macrophage hyper-responsiveness, elevated levels of PGE2 and
IL-1beta in response to bacterial endotoxins.
9. Progressive of attachment loss and bone loss may be selfarresting
10.
Diagnosis based on history, clinical and
radiographic findings
Types:
- Localized: Actinobacillus actinomycetemcomitans
- Generalized: Porphyromonas gingivalis

ACTINOBACILLUS ACTINOMYCETEMCOMITANS
The star-shaped
Etiology of localized aggressive periodontitis
A gram ve bacteria

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By: Sarah Kahil

Course: PERIO511

7/1/2016

A facultative anaerobe can grow under aerobic or anaerobic

conditions
Actinobacillus actinomycetemcomitans from periodontitis patients
releases leukotoxin which kills host white blood cells.

Localized Aggressive
Periodontitis
- Onset around puberty
- Serum antibody response to
infecting agents
- Localized 1st molars/incisors
(interproximal AL affect at
least 2 permanent teeth one
of which is 1 molar) affecting
no more than 2 teeth.

Generalized Aggressive
Periodontitis
- Usually under 30 years or
older
- Poor serum antibody response
to infecting agents.
- Generalized interproximal AL
affecting at least 3 permanent
teeth other than 1st molar and
incisor
- Episodic destruction of
attachment and alveolar bone

LOCALIZED AGGRESSIVE PERIODONTITIS

Clinical Characteristics:
1. Female male
2. Age: between puberty and 20 years
3. Affect 1st molar/ incisor area + interproximal AL on at least 2
permanent teeth. One of which is 1st molars and incisors (i.e 1st
molar should be affected)
4. Lack of clinical inflammation, despite the presence of deep
periodontal destruction
5. Amount of dental plaque inconsistent with amount of periodontal
destruction.
6. Plaque contains increased AA and PG
7. Disto-labial migration of maxillary incisors + diastema formation
8. Increase mobility of teeth
9. Sensitivity of denuded mastication
10.
Periodontal abscess may form + regional LNs

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By: Sarah Kahil

11.

Course: PERIO511

7/1/2016

Progression of AL and bone loss self-arresting

Radiographically:
- Vertical bone loss around 1 molars and incisors
- Arc shaped bone loss extending from distal of 2 nd permanent PMs o
mesial of 2nd permanent molars.
- Gives a characteristic mirror image

N.B: Why are the 1st molars and incisors affected first?
1. Production of adequate immune defenses after initial attack of Aa
to the periodontal sites of 1st permanent teeth to erupt, so
colonization of other sites will be prevented.
2. A.a may be prevented from further colonization via bacterial
antagonist to Aa.
3. A.a may lose its leukotoxins producing ability for unknown reasons
so progression of disease is arrested or retarded.
4. Defect in cement formation responsible for localization of teeth

GENERALIZED AGGRESSIVE PERIODONTITIS

Clinical Characteristics:
1. Usually affect individuals under age of 30 but older patients may
be affected
2. Generalized interproximal AL affecting 3 permanent other than 1 st
permanent molars and incisors
3. Destruction episodic (periods of destruction and periods of
quiescence)
4. Amount of dental plaque inconsistent + amount of periodontal
destruction
5. Plaque contains elevated Pg, Aa and Bacteroides forsythus.
Tannerella forsythia.
6. Produce poor antibody response to pathogens present

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By: Sarah Kahil

Course: PERIO511

7/1/2016

7. Gingival response severe, acutely inflamed (periods of activity) or

gingiva appear pink, free of inflammation despite deep pockets
(periods of quiescence)
Radiographically:
- Serial x-rays will document aggressive nature of disease
- Severe bone loss associated with minimal number of teeth to
advanced bone loss affecting majority of teeth.
Risk factors:
I. Microbial factors:
Increased proportion of AA and Pg
II. Immunological factors:
1. Increased level of human leukocyte antigen (HLA)
2. Presence of functional defects of PMLs and monocytes or both
(impaired chemotaxis and impaired phagocytosis)
3. After T-cell function (helper and suppressor)
III. Genetic Factors:
1. Family history
2. Presence of gene cause
Successful treatment:
- Early diagnosis
- Elimination or suppression of causative micro-organism
- Long term maintenance program
Therapeutic Goals:
- Eliminate the microbial etiology and contributing risk factors
- Arrest/slowdown the progression of disease
- Prevent the recurrence of disease
- Periodontal regeneration
Treatment Consideration:
- Initial therapy
- Antimicrobial therapy with or without surgical management
- Surgical procedures

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By: Sarah Kahil

Course: PERIO511

7/1/2016

- Grafting procedures
Antibiotic Therapy:
- Tetracycline and its derivatives are used
- Systemic antibiotics used as an adjunct to mechanical
debridement
Mechanical therapy + oral hygiene clinically re-assessed after 4-6
weeks (surgery) and antibiotics selection depending on culture
sensitivity tests
- Combination therapy is appropriate
- Recommended to start drug administration immediately
following a mechanical instrumentation.

Surgical Management:
- Surgery is not advisable until there are clinical and microbial
signs of periodontal stability is achieved.
- Monitor every 3-4 weeks is while the disease is in active state.
Outcome assessment:
- Reduction of clinical signs of gingival inflammation
- Reduction of probing depths
- Gain of clinical attachment
- Radiographic evidence of resolution of osseous lesions
REFRACTORY PERIODONTITIS
Not a single disease, because small % of cases of all forms of
periodontitis might not be responsive to treatment, it either:
- Refractory chronic periodontitis
- Refractory aggressive periodontitis
Etiology
1. Abnormal host response
2. Pathogenic virulent bacteria

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By: Sarah Kahil

Course: PERIO511

7/1/2016

3. Failure to eliminate all plaque retentive areas

4. Combination of all these factors
Combination therapy is appropriate.
Recommended to start drug administration immediately following a
mechanical instrumentation.
Referred to cases that do not respond to treatment and/or recur
after adequate treatment.
It should be distinguished from recurrent disease in which a
complete remission occurs after therapy, followed by recurrence
of the disease as a result of reformation of irrational infective
factors, plaque and calculus.

Areas
-

where the periodontal condition does not resolve:

Persistent gingival inflammation
Persistent or increasing probing depths
Progressive loss of clinical attachment
Persistent clinically detectable plaque levels not compatible
with periodontal health
- New involvement of additional teeth and or increasing tooth
mobility in previous treated areas.

In refractory Cases:
Tetracycline-resistant Actinobacillus species suspected.
So combination therapy is preferred
Amoxicillin 375 mg and Metronidazole- 250 mg TID for 7 days

NECROTIZING PERIODONTAL DISEASES

Non AIDs associated:
- Treponema Vicenti
- Fusobacterium nucleatum
- Prevotella intermedia

AIDs associated

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By: Sarah Kahil

Course: PERIO511

7/1/2016

NON-AIDs ASSOCIATED PERIODONTAL DISEASE

Clinical Features:
- Repeated long term episodes of NUG.
- Inflammatory infiltrate extend to underlying bone crater like
osseous defect at IDG
- Conventional periodontal pockets + deep probing depths not
found as ulceration, necrosis destroys marginal epithelium and
CT recession
NUP leads to:
Severe bone loss
Tooth mobility
Tooth loss
Bad odor, fever, malaise, lymphadenopathy
HIV/AIDS ASSOCIATED PERIODONTAL DISEASE
-

Linear gingival erythema

NUG
NUP
Periodontal attachment and bone loss is extremely rapid
Large areas of soft tissue necrosis
Exposure of bone fragments extend to vestibular area and
palate
- Necrotizing ulcerative stomatitis
N.B: NUP in HIV seropositive patients: a sign of <200 microns CD4 +
cells indicate the development of AIDS.
Differs from NUG in low level of spirochetes.
Etiology (increased levels of):
1. Candida albicans
2. Prevotella intermedia
3. Actinobacillus actinomycetemcomitans (Aa)
4. Porphyromonas gingivalis
5. Fusobacterium nucleatum
6. Campylobacter species

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By: Sarah Kahil

Course: PERIO511

7/1/2016

THERAPEUTIC PROTOCOLS FOR NUG AND NUP

- Gentle debridement of necrotic tissue to minimize bleeding and
pain
- Irrigation with 10% Betadine (providone-iodine) to aid
debridement
- If possible scaling and root planing under local anesthesia +
10% Betadine as irrigant.
- Chlorhexidine gluconate 0.12% MR
- Metronidazole or tetracycline 500 mg 4 times/day for 1 week
PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASES
Systemic diseases associated with or predisposed to periodontal
attachment loss:
- Detective number of neutrophils
- Detective neutrophil function
Hematologic Disorders:
- Leukemia
- Acquired neutropenia, agranulocytosis
Genetic Diseases:
- Familial cyclic neutropenia
- Downs syndrome
- Papillon-lefevre syndrome
- Leukocyte adhesion Deficiency syndrome
- Chediac Hegashi syndrome
- Ehler-Danlos syndrome
- Hypophosphatasia
PAPILLON-LEFEVRE SYNDROME
Autosomal recessive inheritance mutations in cathepsin C gene
chromosome 11q14-q21
Characterized by: Palmoplantar hyperkeratosis
- Hyperkeratosis of elbows
- Hyperkeratosis of soles and feet

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By: Sarah Kahil

Course: PERIO511

7/1/2016

- Hyperkeratosis of palms and hands

Severe periodontal destruction with exfoliation of teeth.
Primary and permanent teeth are generally lost in order of
eruption.
Bacterial flora of plaque similar to that of chronic periodontitis.
Immune defects in PMNs
Severe periodontitis with migration of 1ry teeth
Severe alveolar bone destruction

DOWNS SYNDROME (TRISOMY 21, MONGOLISM)

Congenital disease caused by chromosomal abnormalities
Dental deficiency
Growth retardation (hypothyroidism)
Oral

Manifestations:
Macroglossia
Fissured geographic tongue
Hypoplastic teeth
Severe periodontitis deep PP

Destruction around molars and incisors due to:

- Defect in T cell maturation, PMNs chemotaxis
- Increased nr of Prevotella intermedia
NEUTROPENIA
Blood disorder that results in low levels of circulating neutrophils
Causes:
- Genetic
- Drug induced
- Results from viral infection
Affects patients receiving chemotherapy for cancer
It is serious condition
Infections are difficult to manage, life threatening
Periodontal Manifestations:

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By: Sarah Kahil

Course: PERIO511

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- Severe aggressive periodontitis and oral ulceration

HYPOPHOSPHATASIA
Rare disorder due to mutations in tissue-nonspecific alkaline
phosphatase gene
Mutations deficiency in alkaline phosphatase
In abnormal bone mineralization
Skeletal abnormalities
Cement hypoplasia
Premature loss of primary teeth
Infantile form fatal
Mild forms in children and adults
In adolescents resembles localized aggressive periodontitis
Early exfoliation of deciduous teeth and extensive bone loss
CHEDIAK HEGASHI SYNDROME
Rare autosomal recessive inherited disorder
Inherited or congenital defect in phagocytic cell function
Characterized by:
- Recurrent bacterial infections including aggressive periodontitis

LEUKOCYTE ADHESIVE DEFICIENCY

Rare autosomal recessive disease
Begins during or immediately after eruption of teeth
Characterized by:
- Aggressive periodontitis at early age
- Affecting primary and permanent dentition
- Associated with defected neutrophils
- Impaired migration and phagocytosis

EHLER DANLOS SYNDROME

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By: Sarah Kahil

Course: PERIO511

7/1/2016

Autosomal dominant inherited group of diseases, characterized by

impaired collagen synthesis affecting mainly skin and joints
Eleven subtypes with defects in collagen biosynthesis
Type I is the classic form
Type VIII has skin findings similar to type I
Type IV and VIII associated with severe periodontitis of 1 st
dentition
Hyper-elasticity of skin and hypermobile joints
Easy bruising on blowing minor trauma

Oral

Features:
Oral mucosa fragile, bruising
Bleeding after tooth brushing
Gingival bleeding, periodontitis
Wound healing slightly delayed
Hypermobility of TMJ
Patients touch nose with tongue tip
Supernumery or hypodontia
Many caries
Multiple pulp stones on dental radiographs

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