Classification Of Periodontitis (AAP 1999)

Acute Periodontal Diseases (Review this classification in your textbooks)

I. Chronic Periodontitis
1. Acute Necrotizing Periodontal II. Aggressive Periodontitis
Diseases - (ANUG and ANUP)
III. Periodontitis As A Manifestation
2. Acute (Primary) Herpetic Of Systemic Disease
Gingivostomatitis (AHGS)
IV. Necrotizing Periodontal Diseases
3. Periodontal Abscesses and
Pericoronitis V. Abscesses Of The Periodontium
VI. Periodontitis Associated With
ADHP January 2015 Endodontic Lesions
Dr. Weatherford VII. Developmental Or Acquired
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Deformities And Conditions

USE OF THESE POWER POINT HANDOUTS-1

1. Pay attention and “follow”, in sequence, as slides Acute Periodontal Diseases:
are projected and discussed during lecture.
2. Edit any mistakes on handouts and make chan-
ges, additions (i.e. colors), and notes as needed. 1. Acute Necrotizing Periodontal
3. It is deliberate that much text is on slides, but you Diseases - (ANUG and ANUP)
should know more. In after-class study, use the
hand-outs as a study outline and guide. Expand on
and learn the material and also how to APPLY the 2. Acute (Primary) Herpetic
knowledge to patient care. Gingivostomatitis (AHGS)
4. After class, read again and study all the refer-
ences listed on the slides for each section. This 3. Periodontal Abscesses and
includes textbook materials with the referenced Pericoronitis
cases, figures, tables, and exercises, the instru-
mentation modules, the audiovisual material on
the disks and tapes, including those online.
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USE OF THESE POWER POINT HANDOUTS- 2 Acute Necrotizing Periodontal Diseases

5. If small type on a slide is difficult to read, try the 1. FOUNDATIONS OF PERIODONTICS
magnifying devices often found in dental offices.
FOR THE DENTAL HYGIENIST
6. These Power Point handouts are NOT intended as N-G & W - 3
a substitute for other standard sources of dental
hygiene knowledge, but rather for use along side
► Pg 67-80 [Review and find these
these other sources. One such source is the indis-
conditions in the current (1999)
pensable, one-on-one teaching by your dentist -
Classification of Periodontal Diseases]
instructor and other skilled dental professionals.
Other sources are textbooks, lectures, profession-
► Pg 606-609
al literature, various audio-visual material, such
as your and other CD_ROM’s . ►Pg 284-288
7. Early and consistently, make good use of ALL the
oral, printed and electronic sources of in-
formation available to you!!
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1
 Clinical Signs & Symptoms Of ANUG -1
Acute Necrotizing Periodontal Diseases
(See Textbooks for elaboration)
2. CLINICAL PRACTICE OF THE DENTAL A. Intra-Oral
HYGIENIST (W)
1. Pain – rapid, spontaneous, relatively constant

► Pg 651-657 top right 2. Ulceration and necrosis of papillae

► Pg 56 middle left, (Oral Manifestations
of HIV-1) - 57 upper right 3. Bleeding – may be sudden and spontaneous

3. Additionally
► See handouts, including July “Classifca-
tions of Periodontal Diseases” and any
related materials and books. Periodontal,
Dental Hygiene and Pathology textbooks
are good sources for more material on
these topics.
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4. Sudden Onset – Seek help 1-2 days after onset (Acute Pain)
5. Fetor oris (Foul breath)– May or may not. Can be masked
6. Pseudo membrane – Gray film of bacteria, blood, food
sloughed cells etc. Easily removed and thus may not be
seen.
(Diagnosis is suspect if # 1 & # 2 are NOT present)
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Historical Aspects Acute Necrotizing

Ulcerative Gingivitis (ANUG) - 1
► ANUG has been known and described since
ancient times, usually as a disease of young
adults (ages 15-30)
► It was feared and was prevalent in armies, par-
Acute Necrotizing Ulcerative Gingivitis (Early)
ticulaly if living conditions were unsanitary
and crowded. (“Trench mouth” of World War I) Necrosis beginning at tip of papillae (black
arrows) with ulceration of surface epithelium
► Malnutrition, sub-standard living conditions
of marginal gingiva and a pseudo-membrane
and lowered systemic resistance have long
been associated with the occurrence of ANUG. (yellow arrows) of necrotic tissue, fibrin, PMN’s
and microbes. Prominent diagnostic features
► ANUG also has been noted to be superimposed of ANUG include: (1) pain of sudden onset, (2)
over existing periodontitis.
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necrotic punched-out papillae, (3) bleeding.
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Historical Aspects Acute Necrotizing

Ulcerative Gingivitis (ANUG) - 2
► Many synonyms have been applied to this
condition. Among them are:
◘ Necrotizing Ulcerative Gingivitis (NUG)
◘ Acute Necrotizing Ulcerative Gingivostomatitis
◘ Ulcerative Gingivitis
◘ Ulceromembranous Gingivitis
◘ Trench Mouth (World War I “epidemics”)
◘ Vincent’s• gingivitis Acute Necrotizing Ulcerative Gingivitis
◘ Vincent’s• stomatitis Note the clinical features suggested by the
◘ Vincent’s• infection name: The general features of an acute inflam-
matory process of the gingiva (gingivitis), necro-
•(Vincent was an early and prolific worker in the sis of the gingival papillae, and ulceration of the
study of this disorder)
surface epithelium.
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2

Another case of early ANUG showing the clinical
features described on the preceding slide
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Acute Necrotic Ulcerative Gingivitis
Although, the anterior regions are report-
edly more commonly affected, this condit-
ion may occur in any gingival site.
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Clinical Signs & Symptoms Of ANUG -2
(See Textbooks for elaboration)
B. Extra-Oral (May or may not be present)
1. Lymphadenopathy (Usually absent)-- is
swelling and tenderness of lymph nodes
of jaw & neck due to bacterial “filtration.”
and tissue-breakdown products.
2. Slight fever (May or may not be present)
3. Malaise – sense of “not feeling well”.
May be a result of painful gingiva that
prevents proper sleep and nutrition
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Clinical Signs & Symptoms Of ANUG -3
(See Textbooks for elaboration)
C. Tissue Affected & Other Clinical Features
1. Localized to the gingiva normally but may
spread as Vincent’s angina and noma, etc.,
especially if:
a. Malnutrition
b. Lowered resistance or over-burdened
immune systems e.g. children with Downs’
Syndrome (trisomy 21)
2. Disease of young adults in USA. Rare in
children under 10 years unless conditions as
“a”& “b” above
3. Contagion not proven
4. Tissue invasion by spirochetes
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Etiology Of ANUG: Multifactorial -1
(See Textbooks for elaboration)
A. Bacteria (No established specific ones)
1. Fuso-spirochetes are necessary (but also
found in health) and specific tissue changes
are also needed for their effect
B. Local predisposing factors (May produce the
needed tissue changes mentioned above)
1. Existing or localized gingival infections (G’itis)
2. Concurrent injuries of gingiva
C. Systemic predisposing factors (May favor start
of ANUG) (Some of these are inter-related)
(See Systemic Factors# 1-5 listed on
next slide)
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Continued
Etiology Of ANUG: Multifactorial - 2 (Continued)
C. Systemic Predisposing factors (May favor start of
ANUG) ( Some of these are inter-related) (continued)
1. Smoking – Very strong correlation with ANUG. Is
this due to another predisposing factor- such as
stress- that may be independent of smoking, but
which also predisposes to ANUG ??
2. Stress- related or Psychosomatic Factors –
Strong correlations. More negative life events and
loss of social and family support systems. What is
stressful is hard to define > individual variations.
3. Debilitating diseases – Any that lower resistance
may predispose - such as Trisomy 21, Blood
dyscrasias, HIV
4. Nutritional deficiencies – especially of proteins
5. Lack of sleep and rest
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3
 Diagnosis Of ANUG – Based On:
More About the Bacteria of ANUG (See Textbooks for elaboration)
▪ On the surface of the ulcerative lesions, fusiform A. Clinical Signs and Symptoms (See above material)
and spirochete microbes predominate. Key signs and symptoms are:
▪ There is invasion by bactgeria of the non-necrotic 1. Pain
gingiva in ANUG ulcerated leasons up to 400 um. 2. Ulcerated and “punched-out” papillae
*******************************************************
3. Sudden onset in a young adult
Ulcerative Surface
B. History
▪ Bacterial zone 1. Acute (= sudden onset; short, severe course)
▪ Neutrophil (PMN’s)-rich zone 2. Stress – Physically and/or Psychological
Induced
▪ Necrotic zone 3. Other predisposing factors
▪ Zone of spirochete infiltrat- a. Smoking
ion b. Nutritional deficiencies
c. Poor oral hygiene
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Listgarten 1965
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d. Immunocompromised states

Percentage of Cultivatable Bacterial Species Diagnosis Of ANUG :

in ANUG Patients Pre- and Post Treatment
Bacterial Species Pre-TX 2-3 Months Characteristics of ANUG Patients
Post-Tx.
Bacteroides 1. History of smoking
melaninogenicus 26.9% 2.7%
2. History of poor nutrition
Fusobacterium Species 3.1% 0.6% 3. Sudden onset in a young adult
Treponema Species
(Spirochetes) 32.6% 12.4% 4. HIV positive status may be
present
Gram Positive Rods and
Cocci 69% 72%
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Loesche et al. 1982

Clinical (left)
and
Diagnosis Of ANUG – DIFFERENTIAL
photomicro- (See Textbooks for
graph of A. Blood Dyscrasias elaboration)
necrotic Leukemias – Similar oral signs and symptoms
tissue (right)
If the suspected ANUG does not respond quickly
to appropriate treatment, evaluation to rule out
Acute Necrotic Ulcerative blood dyscrasias is mandatory
Gingivitis B. Chronic Desquamative Gingivitis (CDG)
► Note the necrosis, loss of Can tell apart by careful considerations of clinical
structural features, and the features. No papillary necrosis in CDG (Review)
heavy inflammatory cellular C. Acute Herpetic Gingivostomatitis (AHGS)
infiltrate in the microscopic
AHGS occurs more often in children and not limit-
view (upper right)
ed to gingiva – See its clinical features in next
►The bacterial smear (bot- section
tom left) shows a filament- If ANUG does not respond quickly to proper
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ous fusospirochetal flora. TWW
treatment, re-consider your diagnosis !!!

4
 Treatment Of ANUG - 1 Treatment Of ANUG - 4
(See Textbooks for elaboration)
(See Textbooks for elaboration)
C. Correction Of Tissue Deformities of Chronic ANUG
ANUG patients generally respond quickly and (Done After The Acute Phase Has Resolved)
well to appropriate therapy. Therapy may be
►Gingival craters and other deformities may pers-
aimed at the following objectives:
ist enhancing recurrence, which may be 30%.

A. Reduction of Acute Symptoms ► Many patients discontinue treatment when pain

B. Elimination Of Predisposing Factors
C. Correction Of Tissue Deformities of Chronic
ANUG – A later not immediate objective
Specific means of therapy for each of the
above objectives follow – (Next slides)
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lessens, but should return for monitoring and
correction of tissue deformities, as needed.
1. Definitive root planing and curettage
2. Gingivoplasty-
to eliminate soft tissue interdental craters.
3. Osseous Correction – NUP may leave bone
defects
4. Surgical Curettage
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Treatment Of ANUG - 2
(See Textbooks for elaboration)
A. Reduction of Acute Symptoms Designed to
break vicious cycle of pain. See q. 24-48 hours until
acute symptoms are over.
1. Debridement – KEY to success. As soon as possible
, complete as possible, as gentle as possible.
Topical/local anesthesia and nitrous oxide are useful.
Ultrasonics have good lavaging (flushing) effect. Before Treatment After Treatment
2. Medications – Avoid antibiotics unless there is fev-
er and lymphadenopathy. In the rare cases where Acute Necrotic Ulcerative Gingivitis
antibiotics are indicated, metronidazole (Flagyl® is a
►Typical treatment is early thorough debridement,
good choice.
►Mild pain relievers and sleep-inducers, as needed rinses, relief of pain, improved oral hygiene, and
reduction or elimination of predisposing factors.
► Oxygenating rinses (½ strength hydrogen peroxide q.i.d.
► Chlorhexidine rinses – (Alcohol base may “sting”) ► Antibiotics are rarely needed-- and likely never in
3. Oral Hygiene - Stress this. Important to clean. May the absence of systemic signs or symptoms
dip tooth brushes in the rinses prior to use.
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Treatment Of ANUG - 3
(See Textbooks for elaboration)
B. Elimination Of Predisposing Factors.
Careful history to identify them and reduce or eliminate

1. Fatigue & Lack of Sleep.– Get rest. Reduce pain

(Pain may be preventing the patient from sleep & rest.)
2. Smoking – Inform patient. Ask to cease or decrease
3. Localized Injury or Infection – Treat concurrent abs- Before Treatment After Treatment
cess or other local infections &/or systemic diseases.
Acute Necrotic Ulcerative Gingivitis
4. Psychogenic Factors (Stress, etc.) - Lessen if
possible. Be a good, kind, tactful, reassuring listener. Improvement and relief of pain begins within hours
or 1-2 days after typical thorough treatment. If this
5. Diet – Improve. Soft, bland but nutritious. Liquid–diet, does not happen soon, “re-think” the diagnosis and
“Blenderized foods. Multivitamins (not mega-doses)
review the conditions previously considered in the
may be useful
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differential diagnosis.
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5
 ►Gingival craters and loss of
papillae (above) may result from
previous attacks and may predisp-
ose to recurrence. Treatment may
consist of plastic contouring
and/ or regenerative procedures.
► The loss of an interdental papillae
(left) may be a disturbing esthetic
deformity that is very difficult to
correct. Another Case of Necrotic Ulcerative
Periodontitis (NUP)
Gingival Deformities Resulting From ANUG
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Systemic influences
on NUG may include:

◘ HIV conditions
◘ Severe malnutrition
◘ Immunosuppression
due to any cause

Necrotic Ulcerative Periodontitis (NUP)

NUP has clinical features of ANUG, AND also the
distinct features of loss of clinical attachment and
attachment apparatus (i.e. not limited to the Arrows indicate conditions, discussed in this
“Acute Periodontal Disease” section, which
gingiva) in the affected areas. This loss may be are “associated” with HIV infection.
rapid and extensively necrotic in the presence of
aggravating systemic influences. (Consider Perio-
dontal and/or MD referral, especially in these cases)
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Table 4-4. Pg 56 Wilkins Textbook 11 ed.
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►In the U.S.A. necrotic ulcerative

gingivitis is typically a disease of
young adults, but in malnourished
Necrotic Ulcer- or immunosuppressed populat-
ative Periodontitis ions a more severe expression
(NUP) may occur in children or adults.

► One form of this is gangrenous

stomatitis where the infection
may extent beyond the gingiva
to involve other structures,
Other cases of NUP including alveolar bone and the
showing the clinical oral muscles. The process may
appearances and destroy the oral tissues and
appear on the surface skin as a
characteristics large chronic ulcer or other
previously describ- lesions.
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Noma Or Gangrenous Stomatitis
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6

?? QUESTIONS??
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Acute Periodontal Diseases:
1. Acute Necrotizing Periodontal
Diseases - (ANUG and ANUP)
2. Acute (Primary) Herpetic
Gingivostomatitis (AHGS)
3. Periodontal Abscesses and
Pericoronitis
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Acute (Primary) Herpetic
Gingivostomatitis (AHGS)
► Read material referenced on slides
just below and that on the other
following slides.
► Also, read about these conditions in
Periodontal, Dental Hygiene, and
Oral Pathology Textbooks
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Acute (Primary) Herpetic
Gingivostomatitis (AHGS) -1
1. FOUNDATIONS OF PERIODONTICS
FOR THE DENTAL HYGIENIST
N-G & W – 3
► Pg 67-80 (Review and find these
conditions in the current
(1999) Classification of
Periodontal Diseases)
► Pg 610-614
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Acute (Primary) Herpetic
Gingivostomatitis (AHGS) - 2
2. CLINICAL PRACTICE OF THE DENTAL
HYGIENIST (W)
► Pg 657 middle right -659 middle left
► Pg 50 middle right, “Herpesvirus
Diseases”- 52 lower right
► Pg 46-48 Table 4-1 (See especially the
Herpes simplex virus “row” on page
46 of this table)
3. Additionally
► See handouts, and any related materi-
als and books. Periodontal, and Pathology
textbooks are good sources for more
material on these topics.
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Etiology Of AHGS
A. Herpes Viruses
1. Are a large family of viruses characterized by
a. primary infection, b. latent or dormant per-
iods, and c. then chronic secondary attacks
B. Herpes simplex virus
1. Herpes simplex type 1 – Binds primarily to
nerve endings of the oral soft tissues and skin
(above waist) and is the primary cause of AHGS
and some other disorders. ( See following)
2. Herpes simplex type 2 – Primarily affects
genitals, (below waist) although, occasionally
each type may cause the alternate infection.
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7
 See this table 4-3, pg 51, Clinical Signs and Symptoms Of AHGS
Wilkins Textbook, 11th
(See Textbooks for elaboration)
edition.
1. Discrete or clusters of vesicles in initial stage
This table lists the number,
name and abbreviation and 2. Ulcers – Vesicles rupture after 24-48 hours and
usual infections related to produce painful ulcers singularly or in clusters
eight members of the
3. Oral mucosa involvement – Part of gingiva or all of
herpesvirus family.
gingiva and remaining oral mucosa
Today we will consider
4. Skin of face involvement – Usually as herpes
some aspects of the encir-
labialis (“fever blister”; “cold” or “canker” sore)
cled ones, as related to
oral dental infection. 5. Systemic findings – Cervical lymphadenopathy,
(Arrows) fever, malaise and dehydration are not uncommon
in primary attack but are rare in secondary attack
See also tables 4-1 & 4-2
or in ANUG
for more information about
some infectious diseases 6. Duration – Usually 7-14 days duration of an individual
episode, whether it is a primary or secondary attack
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of your patients TWW

See: Figure 4-5 on

page 51, Wilkins
Text-book 11th
edition
Shown here is the
path of the HSV-1
virus from entry
on the lip to laten -
cy in the trigemin-
al ganglion of Cran
-ial Nerve V (Man-
dibular Division)
The different hepesviruses are latent in specific
nerve sites. HSV-1 to trigeminal ganglion; HSV-2
to ganglion of thoracic, lumbar and sacral nerves;
VZV to ganglion of vagal, spinal, or cranial nerves.
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Signs and Symptoms Of Special
Importance to Dental Hygienist
► Oral pain and discomfort
(Instrumentation is likely painful.)
► Difficulty in eating and drinking
► Swollen, red, bleeding gingiva
► Painful oral ulcers on lips, palate, tongue,
and gingival tissues. If severe, may also
have elevated temperature, malaise,
headache, swollen lymph nodes
► Remember that primary herpetic gingivitis
lesions are contagious, especially in the
vesicular stage. Take appropriate
precautions.
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Pathogenesis:
HGS Attacks
Primary Attack
Below age 6 or in
adults without anti-
bodies.
1
Usually subclinical, 2
but may be severe
and generalized, Primary infections of AHGS may
including intraorally.
range from asymptomatic to severe.
‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐ Child #1 has a single tongue vesicle.
Secondary Attack Child #2 has wide- spread mucosal,
gingival and labial lesions. (Touching
Reactivation of the infected area with bare fingers is
latent virus and in-
Life Cycle of Herpes fection and lesions
not recommended)
Simplex Type 1 of epithelium of Child #3 exhibits a severe facial
skin and oral cavity, infection.
(See posted hand-out)
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etc. 3
TWW (From Atlas of Pediatric Emergency Medicine. L Fleisher GR, Ludwig W,
Baskin MN. Lippincott Williams & Wilkins; 2004, Philadelphia)

8
Primary Herpetic Infection in an Infant A very painful, tender
swollen finger caused by
a herpes simplex virus
type 1 infection. The
(From Goodheart HP.
Goodheart's Photo-
guide of Common
Skin Disorders. blisters have many virus
particles, making this
2nd ed. Philadelphia:
Lippincott Williams &
Wilkins; 2003.)
infection highly contag-
ious. Take cautions to
avoid infection through
breaks in your skin or
mucosa and via eyes,
by aerosols and by virus
in saliva. Good hand
This digital infection likely resulted from finger- hygiene by both patients
sucking allowing contact with oral lesions. and clinicians is
Children may also transmit the virus from one important.
site to another (eye, genitals, etc by finger . MARAZZI / SCIENCE PHOTO LIBRARY

contact. TWW TWW

This patient has inflammation of the eyelids due to

a herpes simplex virus infection. Note the red and
swollen eyelids with yellow crusts overlying small
ulcers. The conjunctive --the membrane that covers
Primary Acute Herpetic Gingivostomatitis
the eye and the interior surface of the eyelids-- is
also red and inflamed (“Conjunctivitis”) HOSPITAL / SCIENCE PHOTO
Here the condition is seen atypically in an adult
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LIBRARY

Herpetic Whitlow
or Digital Herpes
► Occur from inocu-
lation from self or
another in the vir-
al transmission
(early) stages of
usually HSV-1 in-
fections Acute Herpetic Gingivostomatitis
► Virus may find en- This is a ten-year old boy with vesicles and
try thru break in
ulcers of the lips (black arrows) and with
skin or torn cuticle.
an erythematous, shiny, edematous,
► Ocular and genital
bleeding marginal gingivitis. This condition
infections may
similarly occur. is painful and this patient is reluctant to
[ whitlow or felon = infection eat and younger children may refuse to eat.
of distal end of finger ]
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9
 Acute Herpetic Gingivostomatitis
This palate exhibits a marginal
In this adolescent patient, there are vesicles of herpetic gingivitis (yellow arrows)
the lip (yellow arrows) in which there are virus
particles and ulcerous areas of the gingiva (black and herpetic ulcers (black arrow)
arrows) that previously were small vesicles.
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of the covering masticatory mucosa.
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► Note the erythematous,

shiny, bleeding, painful
Note the vesicles or marginal gingivitis
“blisters” (above). (yellow arrows) and the
These soon burst after ulcers (green arrows)
that were preceded by
1-2 days, releasing
vesicles that ruptured.
virus particles, and
becoming the encrust- ► The healing tongue
ulcers are large.
ed ulcerated lesion
seen on the right.
TWW Herpetic Gingivostomatitis In A 19-Year Old Female
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Herpes Labialis
This usually represents a secondary attack by the
latent herpetic virus. Secondary attacks are usually
not intraorally, but may occur involving the gingiva
and tongue. Such attacks more commonly occur on
the lips or other structures. The lesion on the left is
a large short-lived vesicle (“fever blister”) that soon
ruptures and to form an ulcer that becomes the
crusty lesion (“cold or canker sore”) seen here on Herpetic Gingivitis Of The Palate
the right.
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10
Herpetic infection of palate showing Acute Herpetic Gingivostomatitis
an erythematous marginal gingivitis The lesions of the primary attack may
and scattered herpetic ulcers affect any intra-oral site as well as the lips.
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Mild Herpetic Gingivostomatitis

There are whitish erosive patches
on the attached gingiva. There is
little plaque and the marginal
gingiva is not greatly inflamed.

Moderate Herpetic Gingivostom-

atitis
Plaque retention is aided by the
orthodontic brackets and plaque-
induced gingivitis is concurrently
present with the herpetic in--
fection.
Severe Herpetic Gingivostoma-
Acute Herpetic Gingivitis of The Palate titis
Note the ulcers resulting from rupture of In addition to the acute gingivo-
stomatitis, there was fever and
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the preceding vesicles TWW lymphadenopathy.

Treatment Of AHGS: General Comments -1

Primary herpetic gingivostomatitis lesions of the
soft palate. Such infections are most commonly
seen on the lips, tongue, gingiva, and oral mucosa.
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CLINICA CLAROS/SCIENCE PHOTO
(See Textbooks for elaboration)
►The condition is self limiting (1-2 weeks) and viral
in origin. So antibiotics are useless unless there is
secondary bacterial infection or the need to pre-
vent such in debilitated patient. Topical steroids
may enhance spread of viral infections (HSV)
► Most treatment is palliative in nature – e.g. to relie-
ve symptoms. Consider treatment with analgesics,
topical anesthetics and protective coatings like
Ora-base® or viscous Lidocaine®, Abreva® etc.
Avoid dentifrices containing sodium lauryl sulfate
►Bed rest, adequate fluids, soft diet supplemented
by proteins especially for compromised patients.
Hospitalization of small child with primary attack?)
► See posted flow-diagram, “Management of Muco-
sitis” of section on Chronic Desquamative Gingivitis
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11
 Treatment Of AHGS: General Comments - 2 Role of the Dental Hygienist in
(See Textbooks for elaboration) Management of HGS - 2
► Antiviral agents that inhibit DNA synthesis, -e.g. 5. Explain to patients that a superimposed bacterial
Valacyclovir (Valtrex®): Acyclovir (Zovirax®) and Infection must be prevented. Show appropriate
others Penciclovir cream (Denavir®) may be con- measures to gently control plaque.
sidered.
Anti-viral agents may be for systemic (oral) or 6. Discus with patients the necessity to eat and
topical (cream) use and are relatively expensive. hydrate well, especially those with painful oral
lesions. Give suggestions about food and liquids.
► Many patients with the usual dental herpetic
lesions present too late –after the prodrome - for 7. Be alert for patients who have repeated severe
systemic antiviral agents to have optimal effect. outbreaks and/or are immunocompromised,
► Systemic antiviral agents may be especially received organ transplants, undergoing chem-
therapy. This should be treated early and aggres-
indicated for immunocompromised patients with
sively and are good candidates for referral for
herpetic infections. Such systemic antiviral
specialty treatment that may require systemic
therapy, if of long duration, might best be done in
antiviral agents.
consultation with appropriate physicians.
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MUCOSITIS Malnutrition
Symp.& Management

Diagnosis Of Acute Herpetic

Xerostomia And Fatigue

Bleeding Pain Infection

Water
(Trauma/Cellular
Warm
Soda/Salt Rinses Candida
albicans
Adequate
hydration Gingivostomatitis
Bottle Q.I.D
Do not Diflucan, Nystatin
near
add to oint., Mycelex

Usually made from the

trauma troches More
frequent small
snacks &
Good Oral meals
Care

1. History
Local areas- Herpes
Sl. pressure Simplex
e.g. Dry tea bag Famvar, Valtrex
20 min on; Acyclovir High- caloric,
Lip Care 20 min off high-protein

and
Products- nutritional
Many® suppl.
Bacterial
Be aware of Depends on results
of the cultures

2. Clinical Findings
& Manage
Sugarless Feeding
Candy/Gum additive
tube - 6-8 cans
causes
nutritional
suppl. daily
Zilactin or
“Artificial Orabase/Benzocaine
Salivas” Be aware Pain Meds-
or “Coatings” for
& Address tablets, Address
single ulcers
2º events exilirs, patches fatique
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From Grandrounds in Oral Syst. Medicine 2/07 p.r.n. Issues
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Role of the Dental Hygienist in Diagnosis Of AHGS– DIFFERENTIAL

Management of HGS - 1 (See Textbooks for elaboration)
1. Be able to explain the pathogenesis and course AHGS may be confused with several conditions,
of the disease – caused by a virus, primary attack especially:
dormant period and then secondary attacks A. Recurrent Aphthous Ulcers (“ Big Canker Sores”)
2. Be aware of the signs and symptoms of HGS and ►Aphthous ulcers are usually on movable
of the differential diagnoses. mucosa and not on gingiva or lips, where
secondary herpetic ulcers are usually found.
3. Know the OTC and other medications used in your ► Aphthous ulcers tend to be larger, more
practice and discuss them with patients. Take solitary, and not preceded by vesicles, as
medications in the prodromal (early) stage compared to herpetic ulcers.
Explain that there is no permanent curative med.
B. Acute Necrotic Ulcerative Gingivitis (ANUG)
4. Educate patients about the contagious stages
► ANUG and AHGS should not be confused if the
of the virus and how to protect themselves and
family – Danger of inoculating self and others – distinct clinical characteristics of each are
touching lesions, applying meds with bare fin- carefully observed and evaluated. (See Tables
gers. Stress importance of good hand hygiene.
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on upcoming slides )
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12
 Comparison Of Acute Necrotizing Ulcerative
Gingivitis And Acute Herpetic Gingivostomatitis (1)

ANUG AHGS

Etiological Not fully establish- Virus - Herpes simplex

Agent ed. Bacteria and type 1
Multiple “factors”
Age Young adults Children and Adults
Two Examples Of Solitary Recurrent Affected usually (in USA) (Primary attacks rare
in adults)
Aphthous Ulcers(“Canker Sores”)
These must be considered in the differential diagno- Gingiva Necrotic papillae Diffuse erythematous
and and gingiva. Pseudo shiny gingivitis.
sis of herpetic ulcers. Aphthous ulcers are usually membrane. Rarely Vesicles of any
on movable mucosa, as shown here on the buccal Mucosa have lesions intraoral site (no
mucosa. They tend to be more solitary and larger Appear- outside gingiva. preferred intraoral site)
than herpetic ulcers. Note the characteristic whit- ance and skin.
ish, grayish ulcer surrounded by fiery red mucosa.
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Comparison Of Acute Necrotizing Ulcerative

Gingivitis And Acute Herpetic Gingivostomatitis (2)
ANUG AHGS

In crops. Rupture to form

Vesicles None clusters of small round
ulcers with red halos
Duration Indefinite. Better 10-14 days. Self-
quickly with Tx limiting
Systemic Usually none Primary attack may have
Symptoms/ : Anorexia, dehydration,
Signs malaise, fever, lymph-
adenopathy
Two Large Aphthous Ulcers on Labial Mucosa
Contagion Not contagious Contagious, especially
Note the grayish ulcer crater surrounded by in vesicle stages
fiery red mucosa that has a raised rim at the Immunity None Primary attack confers
periphery of the ulcers. These lesions are very demonstrated some immunity
painful.
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Multiple Recurrent Minor Aphthous Ulcers
These painful ulcers here are on the soft
palatal mucosa of an HIV-infected patient.
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A table of comparison between necrotizing perio-
dontal diseases and primary herpetic gingivo-
stomatitis from your Wilkins Text 11th ed. Table 41-1
Page 657.
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13
 “Shingles”
Infection Lubinsky Tracy, RDH, MHSc, PHDHP.
on Addressing Primary Herpetic
Posterior Gingivostomatitis in the Dental Office
Chest Wall Dimensions of Dental Hygiene. December
2013;11(12):52–55
http://www.dimensionsofdentalhygiene.com/print.aspx?id=17969
Image Source: Fitzpatrick's Color
Atlas & Synopsis of Clinical
Dermatology Klaus Wolff, Richard
Allen Johnson, Dick Suurmond
Copyright 2005, 2001, 1997, 1993 This is an excellent article that is
comprehensive and practical, published
by The McGraw-Hill Companies

in a journal that is free on asking.

I recommend that you read it and keep it
Herpes zoster (“Shingles”) caused by theVaricella- in a reference file for use when you see
zoster virus (VZV) on skin supplied by right T8 to patients of this kind.
T10 spinal nerves . Vesicles and pustules with eryt-
hema and edema of three contiguous spinal nerve
dermatomes on the posterior chest wall is seen here.
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?? QUESTIONS??
Shingles of Lower Face Caused By the
Varicella –Zoster Virus
The area infected is innervated by which cranial
nerve?? (See Dr Hein’s Anatomy notes) tww

Infectious Mononucleosis
Acute Periodontal Diseases:

1. Acute Necrotizing Periodontal

Diseases - (ANUG and ANUP)

2. Acute (Primary) Herpetic

Gingivostomatitis (AHGS)

Pharyngitis and tonsillitis caused by a herpes virus 3. Periodontal Abscesses and

known as the Epstein-Barr virus (EBV) which also Pericoronitis
causes other infections.
(See Wilkins textbook 11 ed. Pg 51, Table 4-3
Image Collection: Color Atlas & Synopsis of Pediatric Dermatology Kay Shou-Mei Kane, Jen Bissonette Ryder, Richard Allen TWW
Johnson, Howard P. Baden, Alexander Stratigos Copyright 2002 by The McGraw-Hill Companies.

14

Periodontal Abscesses
and
Pericoronitis
► Read material referenced on the slides
just below and that on the other
following slides.
► Also, read about these conditions in
Periodontal, Dental Hygiene, and
Oral Pathology Textbooks
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Periodontal Abscesses and
Pericoronitis
1. FOUNDATIONS OF PERIODONTICS FOR THE
DENTAL HYGIENIST N-G & W – 3
► Pg 67-80 (Review and find these
conditions in the current (1999) of
Periodontal Diseases)
► Pg 597-605- See bottom of pg 602-603 for
“Pericoronitis or Pericoronal Abscess”
2. CLINICAL PRACTICE OF THE DENTAL
HYGIENIST (W)
►Pg 659 middle left - 662
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Periodontal Abscesses and
Pericoronitis
3. FUNDAMENTALS OF PERIODONTAL
INSTRUMENTATION N-G Instr-7
► Pg 548 top (Item b, “Abscess
Formation”)
4. Additionally –
► See handouts, and any related materials
and books that you can. Periodontal,
Dental Hygiene, and Pathology
textbooks are good sources for more
information on these topics
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Etiology and Pathogenesis of Periodontal
Abscess - 1 (See Textbooks for elaboration)
► An abscess of the periodontium is a circumscribed
collection (sac) of pus in the periodontium and is
characterized by pain and swelling. ( Review pur-
ulent exudate or pus)
► Some called those of the gingiva, “gingival” abscess-
es and those in the attachment apparatus, “perio-
donal” abscesses.
► Basic cause is bacteria, (next slide) but their actions
and pus production may be enhanced by “foreign
body” injury (calculus; popcorn husk) or occlusion
(blockage) of pocket opening. This blockage may re-
sult from failure to remove mineralized bacteria (cal-
culus) from the depths of a deep pocket and the ad-
herence of the properly treated coronal aspects of
gingiva to the tooth surface (like pulling the draw-
strings of a bag)
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Etiology and Pathogenesis of Periodontal
Abscess – 2 (See Textbooks for elaboration)
I. Basic Etiology:
► Bacteria – are similar to those in periodontitis
II. Contributing Etiological Factors Include:
► Foreign body injury aiding entry of bacteria
► Incomplete root instrumentation> Closure of
pocket opening & infection persists apically.
► Exacerbation of a chronic pocket lesion
► Systemic diseases that compromise defenses
e.g. Diabetes (Review this in Sept handout)
► Repeated and ineffective use of antibiotics
allowing establishment of a resistant flora
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Etiology and Pathogenesis of Periodontal
Abscess – 3 (See Textbooks for elaboration)
► Periodontal abscesses are usually localized –
i.e. affect one tooth at one time
► For patients who have multiple abscesses at one
time or multiple recurrences at a given site, con-
sider, in addition to local factors, the following:
1. Systemic diseases or Immunocompromised
status . Diabetics mellitus is an example.
2. Patients who have had extensive and
repeated treatments with antibiotics and
may have resistant bacteria
Especially consider (1) and (2) above if the usual
causes for abscesses can not be identified.
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15
 The gingival abscess is
confined to superficial
periodontium (the gingiva)
and is usually smaller and
less symptomatic and relat-
ively easy to treat as com-
pared to the periodontal
Gingival Abscess abscess.
The periodontal abs- Periodontal Abscess
cess affects the deep-
er periodontium (at-
tachment apparatus)
and is larger, more The contents (pus) of this periodontal abscess
symptomatic and more have broken thru the surface establishing a path
difficult to treat than of drainage called a sinus tract (which is some-
times termed a fistula)
the gingival abscess.
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Sinus Tract: Definition

Another Gingival Abscess
Gingival abscesses are relatively rare,
as compared to the more extensive and
destructive periodontal abscesses.
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► A tract leading from a focus of suppuration to a
cutaneous or mucous surface. It usually repre-
sents the path by which the discharge escapes
from an abscess cavity that has been prevented
from closing completely, either from mechanical
causes or from the persistent formation of dis-
charge which must find an exit.
A sinus tract is lined by granulation tissue, and
when it is of long standing the opening may be
dragged below the level of the surrounding surface
by contraction of the scar tissue around it.
(http://manual-of-surgery.com/content/0021-Sinus-and-Fistula.html
► A channel that connects with an abscess or
suppurating area
(Stedman’s Medical Dictionary for the Dental Professions)
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Clinical Signs and Symptoms Of Perio-

dontal Abscess
(See Textbooks for elaboration)
1. Pain and Swelling – This is the usual chief com-
plaint. Pain and swelling decreases when the pus
drains
2. Swollen red gingiva with or without a fistula
3. Tooth may be tender to percussion
4. Radiographic evidence of severe and rapid bone
loss may be seen. BUT this may be absent if the
radiograph is made early in the process
5. Systemic findings – fever, malaise, regional lymph-
adenopathy – As in other acute conditions, these
may or may not be present. Usually are absent in
healthy uncompromised patients.
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Fistula: Definition
► The term “fistul” is from the Latin, meaning “pipe”
or “tube.”
► An abnormal canal passing from a mucous surface
to the skin, e.g. oro-facial fistula, or to another
mucous surface , e.g. oro-antral fistula. Fistulæ
also occur through the epithelium lining one organ
and the epithelium lining another organ, such as
between the bladder and vagina (vesico-vaginal
fistula), or between the rectum and the bladder
(recto-vesical fistula).
(http://manual-of-surgery.com/content/0021-Sinus-and-Fistula.html
► An abnormal passage from one epithelial surface
to another epithelial surface.
(Stedman’s Medical Dictionary for the Dental Professions)
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16

Periodontal Abscesses
Two examples of acute periodontal abscesses.
On the left, the probe demonstrates a commu-
nication from the sulcus to the circumscribed
collection of pus that characterizes abscesses.
Both of these patients presented with the
characteristic chief complaint of “pain and
swelling”.
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Periodontal Abscesses
► The expansion of the pus that all abscesses
produce is influenced by the structure of the
tissues of the region.
► The loose alveolar mucosa on the left allows a
large swelling, but the tight palatal masticat-
ory mucosa of the patient on the right results
in a more circumscribed smaller swelling.
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Periodontal Abscesses
►Many kinds of foreign bodies
may initiate periodontal
abscesses. Pop corn husks
are commonly blamed. Here
a husk (red arrows) was
expelled from a small recent
abscess.
► A subgingivally displaced
orthodontic elastic (black
arrow is removed from a
chronic abscess.
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The Dental Hygienist
and Early Intervention
► Early intervention of emergency
periodontal conditions, and especially
in the case of abscesses can limit
permanent damage.
► Dental hygienists may see the early
stages of emergency conditions in pat-
ients presenting for their routine treat-
ment and recall appointments and
should be alert and initiate early
treatment.
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Treatment Of Periodontal Abscesses - 1
(See Textbooks for elaboration)
A. Treatment of ACUTE phase
1. Drain promptly:
a. Through sulcus by curettage and root
planing
b. Incision (stab the surface) and drainage (I
and D)
c. Via flap access
2. Topical (local delivery) antibiotics into the
“cavity" of the abscess
3. Systemic antibiotics – Usually not indicated.
Consider only if there are systemic signs
and symptoms
4. Occlusal adjustment, if indicated, of involved
tooth
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Continued
Treatment Of Periodontal Abscesses -2
(See Textbooks for elaboration)
(Continued)
B. Treatment of CHRONIC phase
1. Follow and monitor abscessed site until
there is complete resolution
2. Discover and manage predisposing and
concurrent periodontal and systemic
diseases
Abscesses are often associated with deep
pockets and periodontitis of which the
patient was not previously aware.
Therefore, examine, diagnosis, inform and
treat as indicated.
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17
 I. Drainage
via pocket
orifice
using a
curette
(red
arrow)
II. Drainage through the
surface gingival wall using
a curette (black arrows)
Treatment of Periodontal
Abscesses
The basic principle of treatment is to estab-
lish drainage by one of several methods.
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Treatment Of Periodontal Abscess Via A Flap
Drainage of Periodontal
Abscesses
Here drainage is accomp-
lished by a scalpel incision
through the surface of the
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gingiva.
Use Of Drains In Treatment Of Abscesses
A T-shaped drain, cut from rubber dam mater-
ial, is inserted (yellow arrows) to maintain
the patency (opening) of the incision and to
insure continued drainage. Other methods of
using drains are also available.
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Treatment Of Periodontal Abscess Via A Flap
A flap is reflected by a semilunar
incision in the alveolar mucosa to
reach the cavity of the abscess.
An alternative is to reflect the flap
from the gingival margin
The pus is drained and the inflam-
matory tissues are removed. The
area is irrigated and inspected.
The tissues are loosely approxi-
mated by sutures. Drains may be
inserted in large abscesses to
ensure continued drainage.
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The patient presented with pain and swelling
(left arrows). Reflection of an envelope flap
revealed that the abscess had invaded the
furcation and penetrated through the cortical
plate (right arrows). The site was curetted well,
irrigated, and the flap sutured in place.
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Management of The Chronic Phase
of Periodontal Abscesses
►Abscess often occur in deep chronic periodontal
pockets that may persist, in the affected or other
teeth, after the acute phase of the abscess is
managed.
► The abscess may be the patient’s first aware-
ness (“wake-up call”) of periodontal “problems.”
► If conditions favoring abscess formation remain,
recurrence is likely.
►Thus - explain to the patient the extent of the pro-
blem and offer the opportunity for evaluation and
necessary treatment beyond the relief of pain of
the acute phase of the presenting abscess.
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18
 Diagnosis and Prognosis Of Periodontal Abscess Differential Diagnosis
(See Textbooks for elaboration) Acute (Endo,
Finding Periodontal
A. Diagnosis Pulpal) Periapical
Abscess
Abscess
► An abscess is generally easy to diagnose based
on the clinical picture. The “hard” basic quest- Probing Periodontal No periodontal
ion may be: “Is the abscess one of the perio- Pocket pocket
dontium or of the pulp ( = pulpal, periapical, Swelling Localized and May be larger and
endodontic abscess)??” Are both affected ?? coronally more apically
(See table of differential diagnosis for help.)
B. Prognosis Fistula (if
present) More coronally More apically
► This is dependent on (1) the amount of attach-
ment lost and (2) ability to control the infection. Vitality of
tooth More likely vital Less likely vital
► Prognosis is generally good if (1) the process is
acute, not chronic; (2) destruction is not ex- Evidence of
ceasive; (3) treatment is prompt and adequate. Less likely More likely
caries
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Periodontal Abscess Differentiated from Not All Swellings With Or Without

Periapical (Pulpal) Abscess
Pain Are Abscesses
Perio abscess Deep Perio-
in this area dontal. Abscess
with 2 drainage
points
☜
Pulpal abscess
in this area and/or

►The patient on the left presented with a “sudden

► Periodontal abscesses (left and middle above) are non-painful swelling” (black arrow) that is a torus.
associated with pockets and drain via the pocket
► The patient on the right presented with “pain
and/or through the more coronal cortical plates.
and swelling”. The swelling (black arrow) is a
► Pulpal (or periapical or endodontic abscesses) torus and the pain was due to trauma exposing
drain thru more apical cortical plates (left above)
TWW the more anterior cortical bone (yellow arrow).
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Accessory (Lateral) Pulpal Canals

(See Textbooks for elaboration & anatomy lectures on accessory pulp canals)

► These run from the main root

canal to exit on the surfaces of Pericoronitis
the roots. 1
► They may provide a route for an 2
infection to move from :
A Variety or Type of
(1) A carious lesion in the
pulp to a periodontal
Periodontal Abscesses ??
defect (yellow arrow). (Sometimes it is called a
(2) A periodontal pocket to
the pulp (black arrow). Pericoronal Abscess)
► Open accessory canals may be the basis for
some combined periodontal/endodontic problems
(yellow circle).
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19
 Pericoronitis: General
► Pericoronitis (=around + crown + inflammation)
- defined as inflammation of the gingiva
surrounding the crown of (usually) a partially
erupted tooth, which is almost always a
mandibular molar. The inflammation is caused
by an acute bacterial infection.

► The clinical features (acuteness, pain, inflam-

mation, and swelling with purulence ), the
etiology, and methods of treatment are similar
to those of periodontal abscesses.
► Sometimes, a molar of the opposing arch may
impinge on and traumatize the swollen pericorn-
al tissues, adding to the severity of symptoms
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Pericoronitis of A Partially
Impacted Third Molar
Note the operculum or “lid” of gingiva that covers
part of the occlusal surface and provides a good
hiding and incubating site for bacteria.
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Pericoronitis: Signs and Symptoms Pericoronitis: Clinical Features - 2

► Red, swollen, tender suppurating, pericoronal ► Note the swollen
tissues usually associated with partially pericoronal tissues
erupted crown. (A projection of the soft tissue around the third
over the occlusal surface of the tooth is called molar
an operculum (opercul = lid or cover)
► A mirror view of a
► Pain may radiate to ear, throat and floor of large pericoronal in-
mouth flammation of a part-
ially erupted molar.
► May be limitation of ability to open (trismus)

► May occasionally have systemic features in ► The small arrows

severe cases – fever, malaise (vague feeling of point to “indentati-
not being well), fatigue and lymphadenopathy ions” that may be due
(swollen, tender lymph nodes of the region) to the striking cusps
of an upper molar.
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Pericoronitis: Clinical Features - 1 Treatment of Pericoronitis: Acute Stage - 1

► Depends on severity of inflammation, sys-

temic complications, and advisability of
retaining the involved tooth
► Cleanse area, establish drainage (as for
periodontal abscess), irrigate well with
warm saline or antiseptic of choice. May
place a drain of iodoform gauze or rubber
“T drain”

► If systemic involvement – consider antibio-

Note the inflamed, swollen
discolored tender pericoro-
nal tissues. (Arrows point to
TWW
the operculum
tics, e.g. broad spectrum penicillin-type
► If opposing tooth is traumatizing – consider
selective grinding of its cusps or extraction
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20
Treatment of Pericoronitis: Acute Stage - 2
►The treatment is Please see the POSTED documents entitled:
essentially that for the
periodontal abscess with “Life Cycle Of Herpes Simplex Type 1”
some modifications as (Enlargement of Slide #45)
listed on the previous
slide. See the two Word documents named below,
placed in last section, but which are also
► The site is cleansed and pertinent to some conditions in this section:
drainage established
Curettage, Drainage, Irrigation
usually with a curette
and Follow-Up 1. “Mucositis: Symptomatic Management”
through the sulcus as
shown here. Thorough (This is a “flow chart”)
irrigation is done and
appropriate prescript- 2. “Common Superficial Oral Lesions-
ions – analgesics, anti- Table I”
biotics(?) are provided.
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Treatment of Pericoronitis: Chronic Stage -1

► After acute symptoms have subsided, decide

either to retain or extract the involved tooth.
► Above decision may depend on (a) likelihood of
further eruption into a good functional position
and (b) possibility of bone loss distal to the 2nd
(adjacent) molar being caused by the extraction
► Surgical reduction of the pericoronal tissues may
?? QUESTIONS??
be done if the tooth is to be retained. Surgery
may be done now or waiting until a (but only one)
recurrence of the pericoronitis.
► Consider selective grinding of the cusps or ex-
traction of an opposing tooth -- if it is “hitting”
the tender pericoronitis site.
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Treatment of Pericoronitis: Chronic Stage - 2

► If the decision is to retain
the tooth ( see previous
slide) and particularly, if
there have been recur-
rences, surgical removal
of excessive tissues may
be done.
Gingivectomy
of distal pocket
► This can be accomp-
lished by gingivectomy
(to left) or by a distal
wedge flap procedure.
The aim is to remove the
tissue that provided a
sheltered site for
TWW The desired result bacteria to colonize.

21