Periodontal Diseases and Disorders - University of Maryland School

SESSION PLAN
COURSE # AND TITLE:
PEDS 538, Pediatric Dentistry
SESSION # AND TOPIC:
# 10 Periodontal Disease and Assessment in
Children. Other Oral Problems, and Oral
Manifestation of Disease
DURATION:
Equivalent to 1 hour
FACULTY:
Dr. Glenn Minah
GENERAL GOALS:
Become familiar with various soft tissue
abnormalities and diseases found in children
SPECIFIC OBJECTIVES:
The student should be able to:
1. Discuss the etiology, clinical appearance and
treatment of pericoronitis, pre-pubertal
periodontitis, localized juvenile periodontitis,
NUG and gingival hyperplasia.
SESSION PLAN
SPECIFIC OBJECTIVES:
The student should be able to:
2. Discuss the etiology, clinical appearance
and implications regarding dental treatment
for herpetic gingivostomatitis, recurrent
herpes simplex, varicella-zoster,
herpangina, impetigo, hand, foot and mouth
disease, candidosis, scarlet fever and certain
systemic diseases.
METHODOLOGY:
Web Lecture
ASSIGNMENT:
McDonald RE, Avery DR. Dentistry for the Child
and Adolescent. Mosby, St. Louis, 7th ed. 2000.
Chapter 20, p.440
EVALUATION:
Written exam. Questions will come form the text
portion of this presentation.
TEXT
SESSION OUTLINE
A.
B.
Periodontal conditions
1.
Child versus adult periodontium
2.
Gingivitis
3.
Periodontitis
4.
Other
Other oral mucosal lesions
1.
Viral infections
2.
Bacterial infections
3.
Fungal infections
4.
Systemic disorders with oral manifestations
TEXT
Periodontal Diseases and Disorders
1.
Child versus adult periodontium: In the child: 1) The interdental papillae are
larger. 2) The gingival margins are less sharp and the tissue is thinner, less tight
and may appear more erythematous. 3) Pseudopockets are often present due to
partially erupting teeth. (Sulcular depth in healthy crevices may be slightly deeper
than in adults, i.e., ~1.0mm.) 4) Plaque levels often do not correlate with
gingivitis. It is not uncommon to observe abundant plaque with little or no
gingivitis.
2.
Chronic gingivitis: Chronic gingivitis is more of a problem in teens than in
children with early mixed or primary dentitions. In teens, careful periodontal
examination is necessary since early onset periodontal diseases can be easily
overlooked. Plaque control should be a prevention priority since many teens
develop periodontitis at an early age.
PERIODONTAL DISORDERS
Adult versus child:
adult
child
adult
Adults show longer interdental
papillae.
child
adult
The adult in health vs a
child has shallower
crevice depths and
tighter denser gingivae
child
Adult gingivae shows
inflammatory changes with plaque
build-up, but the child’s frequently
does not.
ADULT
CHILD
CHRONIC GINGIVITIS
Tissue response to plaque:
CHILD
ADULT
TEXT
Periodontal Disease and Disorders
3.
4.
Pericoronitis: Pericoronitis is a localized infection characterized by gingival
inflammation and often systemic sequelae which accompany a partially erupted
tooth (usually permanent and most commonly 3rd molars). If fever and local
lymph node swelling are evident, systemic antibiotics are indicated. Patients
should also rinse 2 to 3 times daily with astringent mouthrinses (warm saline or
commercial mouthrinse).
Eruption gingivitis: This occurs around erupting teeth due to non-physiologic
position of emerging crowns and adjacent gingivae. When teeth are fully
erupted, cervical contours will shield tissue from food impaction or other
masticatory trauma. Treatment is seldom necessary.
PERIODONTAL DISORDERS
Pericoronitis:
Treatment:
If systemic signs of
inflammation are present
antibiotics are indicated.
Saline or commercial
mouthwashing is beneficial.
This often
accompanies 3rd
molar eruption.
PERIDEX
0.1%
SALT
ERUPTION PROBLEMS
Mastication
trauma
Eruption
gingivitis
Eruption cyst
TEXT
Periodontal Disease and Disorders
5.
Necrotizing ulcerative gingivitis (NUG): This disease occurs ordinarily
in young adults, but the population may include teenagers. Symptoms
and clinical findings are 1) oral pain upon eating or brushing teeth, 2)
interdental ulceration in area of mandibular incisors (usually) with
pseudo-membrane covering affected tissue, 3) characteristic fetid breath
and 4) low fever. The etiology of NUG is not clearly understood, but
involves stress and anaerobic bacteria among which Treponema species
(spirochetes) are the predominant microorganisms in the lesions and will
invade superficial connective tissue. A viral etiology has also been
proposed. The disease is self-limiting and persists for 10 to14 days.
Debridement of affected areas and antibiotics may enhance resolution.
Necrotizing Ulcerative Gingivitis (NUG)
NUG
1.
Pain upon eating
or brushing
2.
Interdental
ulceration
3.
Fetid breath
4.
Slight
temperature
spirochetes invade
connective tissue.
Treatment:
Darkfield
microscopy
indicates that
spirochetes
dominate the flora
PEN or MET reduces
time-course of
infection. Both kill
spirochetes.
TEXT
Periodontal Disease and Disorders
6.
Hormonal gingivitis: This appears during the second trimester of pregnancy and
during puberty. In both cases gingival inflammation is caused indirectly by
excessive sex hormones in the circulation. These act as ecological determinants for
certain oral anaerobic bacteria (e.g., Prevotella intermedia) which become more
numerous in plaque and induce gingival inflammation which can sometimes be
acute. Plaque control and Peridex mouthrinses (0.1% chlorhexidine) 2x/day are
recommended.
HORMONAL GINGIVITIS
estradiol
Pregnancy, puberty
gingivitis
PERIDEX
Puberty
gingivitis
0.1%
testosterone
P. intermedia
TEXT
Periodontal Disease and Disorders
7.
Phenytoin-induced gingivitis (Dilantin hyperplasia): This condition often
accompanies phenytoin administration which is used to control epileptic
seizures, appearing in 40 to 50% of drug recipients. It may also develop with
administration of calcium channel blockers and cyclosporins. Clinically it
appears as gingival overgrowths with low levels of inflammation, but the
tissue is not hyperplastic, histologically. Severity may be related to dose of
dilantin, but genetic predisposition is also suspected. Gingival surgery is
recommended in extreme case (where mastication of tissue occurs) and
extraction of teeth will eliminate the overgrowth at the extraction site. Plaque
control will help reduce tissue growth and cessation of the medication will
cause reversal of the condition. Other treatments are topical administration of
folic acid, topical vancomycin and positive pressure appliances.
PHENYTOIN-INDUCED GINGIVITIS
Dilantin Hyperplasia:
1.
Tissue is not
hyperplastic and
responds to presence
or absence of plaque
and to dose of
Dilantin.
2.
Genetic
predisposition is
suspected.
3.
Treatments include a)
gingival surgery, b)
folic acid, c) topical
vancomycin or d)
positive pressure
appliances.
4.
Calcium channel
blockers and
cyclosporins also may
cause the condition.
Periodontal Disease and Disorders
TEXT
8.
Localized juvenile periodontitis (LJP): LJP is a form of aggressive periodontitis
which affects up to 1% of 12 to 16 year olds. It is characterized by rapid
periodontal pocketing at incisor and molar sites, low tissue inflammation and
plaque levels and low caries rates. The etiology is related to high plaque levels of
Actinobacillus actinomycetemcomitans (Aa) and immune defects (impaired
chemotaxis) and occurs often in family members of the patient (thought to be
genetically related). Treatments consist of periodontal scaling, systemic
tetracycline and local irrigation with either Peridex (0.1% chlorhexidine), a
baking soda-salt-hydrogen peroxide solution or chloramine T. (Careful
periodontal probing should be conducted routinely in teens, as LJP may be easily
overlooked.)
9.
Pre-pubertal periodontitis (PPP): This is aggressive periodontitis which differs
from LJP in that it affects the primary dentition (patients younger than 12), Aa is
not as prevalent and pocketing may be localized or generalized. Genetic immune
defects are usually present and familial patterns of occurrence are observed.
Treatment is similar to LJP. PPP also is part of Papillion-Lefevre syndrome (PL)
wherein planar hyper-keratosis of palms along with PPP are distinctive
symptoms. PL is caused by an autosomal recessive genetic abnormality.
AGGRESSIVE PERIODONTITIS
PPP
LJP
RPP
AP, Chronic
Age
<12
12-16
16-35
>35
Plaque
Low
Low
Low/high
high
Caries
Low
Low
Low/high
normal
Teeth
affected
All
Incisors
and
molars
All
all
Host defects
Yes
Yes
?
no
Pathogens
?
Aa
?
Pg
spirochetes
Aa
Genetic
Yes
Yes
?
no
M/F ratio
1:1
3:1
3:1
1:1
Localized (L)
Generalized
(G) bone loss
L, G
L
L, G
L, G
LOCALIZED JUVENILE PERIODONTITIS, LJP (Old terminology)
Vertical
bone loss
around
molars and
incisors.
LEUKOTOXIN
Aa
Aa secretes
leukotoxin which
kills leukocytes
High levels of
Aa in pockets
Treatment:
PMN
chemotaxis is
impaired
(genetic defect)
Antibiotics – TET,
MET
scaling
LOCALIZED JUVENILE PERIODONTITIS (LJP)
Extruding Tooth
LJP
Actinobacillus
actinomycetemcomitans
(Aa)
Monoinfection of Aa in
germ-free rat
PRE-PUBERTAL PERIODONTITIS (Old terminology)
PRE-PUBERTAL PERIODONTITIS
TEXT
Periodontal Disease and Disorders
10.
11.
Gingival recession: This occurs in regions of mandibular or maxillary
incisors. Causes are 1) a narrow band of attached gingiva, 2) high frenum
attachment, 3) malocclusion, 4) deep bite and, rarely in children, 5)
periodontitis. Treatment consists of appropriate surgery, scaling and/or
orthodontics.
High frenum attachments: In addition to gingival recession, these may cause
diastemas or speech impediments.
GINGIVAL RECESSION
From a deep overbite
From fingernail trauma
High frenum attachment
Abnormal lingual frenum attachment
causes “tongue-tie” and speech problems
Condition
Common
occurence
Less common
Periodontal
Chronic gingivitis
a
Periocoronitis
a
Eruption gingivitis
a
NUG
a
Hormonal gingivitis
a
Dilantin
hyperplasia
a
LJP
a
PPP
a
High frenum
attachment
a
Viral Infections
1.
TEXT
Acute herpetic gingivo-stomatitis (primary herpes infection): Primary herpes is a
viral infection of the oral mucosa caused by Type I herpes simplex virus (HSV-1). It
affects young children (usually under 5 years) who have not developed resistance to
the virus. Clinically, patients present with multiple painful ulcers, 1 to 2mm in
diameter surrounded by erythematous tissue on all mucosal surfaces of the oral cavity.
Pain upon eating, especially salty or acidic foods, is common and tooth-brushing is
painful if ulcers appear on gingivae. Low fever and malaise also are present and
patients often become under-nourished or dehydrated from insufficient food or
liquids. The infection which sheds viruses from ulcers, is highly contagious and can
spread to other mucous membranes such as eye tissue. The condition is self-limiting
and will subside within 10 to 14 days. Palliative treatment includes topical viscous
xylocaine or benadryl elixir plus kaopectate (to relieve for pain, especially upon
eating) and Pedelite, a balanced nutrient drink to compensate for insufficient diets.
Acylovir (Zovirax; 400mg q3h for 10 days) may be administered in extreme cases to
inhibit the virus. (Note: steroids should not be used as the inflammatory reaction
constitutes the first line of defense against the virus.) Differential diagnosis must rule
out candidaisis (thrush) which is not painful and produces a white membranous
patches on mucosal surfaces.
VIRAL INFECTIONS
Primary herpes infection:
Symptoms:
1.
Painful generalized
ulcers on oral
mucosa. Sometimes
it appears extraorally.
2.
Low fever and
malaise. Patients
often are undernourished due to
pain upon eating.
3.
Self-limiting. Will
last 10 to 14 days.
Occurs frequently
in young children
VIRAL INFECTIONS
Primary herpes infection:
Treatment:
1.
Palliative treatment
2.
Viscous topical
anesthetic.
3.
Nutrient supplements.
4.
Acyclovir (anti-viral
agent)
VIRAL INFECTIONS
Primary herpes infection:
Cause: Herpes
simples virus, type
1 (HSV-1)
Transformation to
lytic form. Virus
destroys cell and
is shed.
mucosa
cytolytic
Latent
form.
Viral
genes
combine
with host
DNA
nucleus
Viral Infections
2.
TEXT
Recurrent herpes labialis (cold sore): This is a HSV-1 infection which
occurs in individuals who previously experienced a primary herpes
infection. The virus remains dormant in sensory nerve ganglia after the
first infection, but can erupt following episodes of emotional stress,
excessive exposure to sunlight, trauma, dental procedures or intake of
certain foods to form single ulcerated lesions on the vermilion border of
the lips and mouth (usually). The common occurrence during “cold
seasons” when resistance is often compromised accounts for the name
(cold sore). In addition, foods containing high levels of arginine such as
cereals, nuts and chocolate can activate the virus. The limited
manifestation, versus primary herpes, is due to immunity developed after
the first exposure to the virus. The condition is self-limiting, lasting 10 to
14 days. Remedies which may enhance resolution of the ulcer are alloe or
acyclovir which inhibit HSV-1. Foods high in lysine such dairy products
and yeast may alleviate the condition by counteracting the effect of
arginine.
VIRAL INFECTIONS
Recurrent herpes labialis:
After a primary infection HSV-1
travels up a sensory nerve and
remains dormant in a ganglion
(trigeminal).
It can revert to the lytic form
upon certain stimulation and
usually erupts at the vermillion
border of the lips.
Viral Infections
TEXT
3.
Herpangina: This is caused by the cocksackie A virus and is evidenced by
multiple painful ulcers on oral mucosa similar to primary herpes infections. The
susceptible age is similar to that of primary herpes, being before age 5, but it is
less common and affects mainly the distal portion of the mouth or throat.
Treatment and progress of the condition is similar to that of primary herpes.
4.
Hand, foot and mouth disease: The causative agent is cocksackie A virus and
clinical appearance is herpetic-like multiple ulcers on the hard palate, tongue
and buccal mucosa. The susceptible ages are 1 to 10 years and the condition is
less common than primary herpes. In addition, characteristic ulcerative lesions
appear on soles of feet and plams. Treatment and course of the disease are
similar to primary herpes.
5.
Herpes zoster infection (varicella zoster virus, Type 3 Herpes Simplex virus):
This is commonly known as chicken pox when it affects school age children
and first appears as papular lesions on the skin which form encrusted ulcers. If
the virus infects adults, shingles, a painful dermal condition, will develop. In
chicken pox oral lesions appear on oral mucosa secondarily to skin lesions and
resemble herpetic ulcers, but are not painful (usually). The disease confers
immunity and is self-limiting within 14 days.
VIRAL INFECTIONS
Varicella (chicken pox) –
zoster (shingles). Human
Herpes Virus-3; HHV-3:
Coxsackie A virus:
Herpangina
chickenpox
shingles
Hand foot and mouth disease
Bacterial Infections
1.
2.
TEXT
Impetigo: This is typified by dermal lesions on face or extremities
and often affects groins and axillae. Lesions, which may be either
bullous (blisters which rupture) or non-bullous (smaller and
encrusted) are highly contagious. The causative agent of bullous
lesions is Staphylococcus aureus and of non-bullous lesions is Group
A, hemolytic streptococcus. Topical or systemic antibiotics are the
customary treatment.
Scarlet fever: Scarlet fever is an infection by group A streptococci
(Streptococcus pyogenes) and is characterized by a bright red papular
rash on the trunk. In the oral cavity “strawberry tongue” is common
which is a red tongue covered by a removable coating and presence of
distinctive swollen papilla. Treatment consists of systemic antibiotic
regimens and complications include rheumatic fever, arthritis and
glomerulonephritis.
BACTERIAL INFECTIONS
Impetigo:
The ruptured blister,
encrusted lesions are caused
by beta hemolytic Group A
streptococci.
The bullous lesions are
caused by
Staphylococcus aureus
impetigo
TEXT
Fungal Infections
Candidosis (thrush) is the most common oral fungal infection and
frequently affects young children. It appears as white patchy lesions on
the oral mucosa. When the white patches are removed a bright red
tissue surface is seen which is usually non-painful. Sometimes a
distinctive yeasty oral odor is present. Occurrence frequently follows
broad spectrum antibiotics, but it may also be transmitted from vaginal
yeast infections. Diagnosis may be confirmed by identification of
Candida albicans in mucosal specimens and treatment consists of
topical anti-fungal ointment such as Nystatin.
FUNGAL INFECTIONS
Candidosis (Thrush):
“thrush”, “acute pseudomembraneous”
TREATMENT
Cell wall with no
peptidoglycan
Yeast cell
Cell membrane
POLYENES
ergosterol
• nystatin
• Amphotercin B
AZOLES
These adsorb to
• miconazole
cell membranes
• fluconazole
and disrupt
• ketoconazole
ergosterols
These inhibit
synthesis of
ergosterols
Condition
Common
occurence
Less common
Viral
Primary herpes
a
Secondary herpes
a
Herpangina
a
Hand, foot and
mouth
a
Chicken pox
a
Bacterial
Impetigo
a
Scarlet fever
a
Fungal
Thrush
a
TEXT
Recurrent Aphthous Ulcer (canker sore)
This appears as single (usually) painful erythematous ulcers on oral
mucous membranes which are slightly larger than herpetic lesions.
The condition is self-limiting within 14 days, but contains no virus.
The etiology has not been definitively established, but may involve
autoimmune reactions to antigens from Streptococcus sanguis.
Several palliative non-prescription remedies are available including
kenalog in orabase (a steroid anti-inflammatory agent; Note: steroids
may be used since viral etiology is not suspected.)
RECURRENT APHTHOUS ULCER (CANKER SORE)
The condition is self-limiting
and is treated by palliative
measures.
A definitive cause is not
known.
Systemic Disorders with Oral Manifestations
TEXT
1.
Diabetes mellitus (Type 1, insulin dependent): Oral manifestations are 1) high
salivary glucose concentrations (>120mg/100ml; normal >80mg/100ml), which
may cause increased dental caries rates, 2) LJP-like periodontitis, 3) intra-oral
abscesses, 4) hypo-salivation and 5) yeast infections.
2.
Acute lymphocytic leukemia (ALL): This is one of the most common
malignancies affecting children (occurrence = 4 in 100,000). Oral
manifestations include 1) exudation from gingivae, 2) hematomas, 3)
lymphadenopathy, 4) oral ulceration and 5) pharyngitis.
3.
Acquired immunodeficiency syndrome (AIDS): Oral manifestations are 1)
thrush (this may appear before AIDS is apparent), 2) parotid swelling, 3) acute
marginal gingivitis (appears commonly on the facial) and 4) herpetic ulceration
on mucosal surfaces. HIV and AIDS in children stem largely from maternal
transmission during birth and secondarily from blood transfusions. Children
often develop Pneumocystis carnii pneumonia and exhibit high counts of CD4
lymphocytes.
SYSTEMIC DISORDERS WITH ORAL
MANIFESTATIONS
Diabetes:
Acute lymphocytic leukemia:
1.
1.
Exudations from gingivae
2.
Hematomas
3.
Lymphadenopathy
4.
Oral ulceration
5.
Pharyngitis
High salivary
glucose = caries
2.
LJP-like
periodontitis
3.
Intraoral
abscesses
4.
Hyposalivation
5.
Yeast infections
SYSTEMIC DISORDERS WITH ORAL
MANIFESTATIONS
AIDS:
Parotid swelling
thrush
gingivitis
periodontitis
Herpetic ulceration
SYSTEMIC DISORDERS WITH ORAL
MANIFESTATIONS
AIDS:
AIDS periodontitis
AIDS gingivitis
Parotitis
Condition
Common
occurence
Less common
Other
Aphthous ulcer
a
Systemic
Diabetes
a
ALL
a
AIDS
a
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