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Chapter 4
Infectious Diseases
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
Outline
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Bacterial Infections
Fungal Infections
Viral Infections
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Bacterial Infections
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Impetigo
Tonsillitis and Pharyngitis
Tuberculosis
Actinomycosis
Syphilis
Necrotizing Ulcerative Gingivits
Pericoronitis
Acute Osteomyelitis
Chronic Osteomyelitis
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Infectious Diseases
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(pg. 119)
We are surrounded and inhabited by an
enormous number of microorganisms.
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Whether the organisms cause disease
depends on the microorganism and the body’s
defenses.
Traditionally, the microorganisms are divided
according to whether they are disease causing
(pathogenic) or non–disease causing
(nonpathogenic).
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Infectious Diseases (cont.)
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
The oral cavity may be the primary site of
involvement of an infectious disease, or a
systemic infection may have oral
manifestations.
There are different routes of infection.

Transferred through the air on dust particles or
water droplets
 Some may require intimate and direct contact.
 Some may be transferred by hands or objects.
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Infectious Diseases (cont.)

Microorganisms invading oral tissue can
cause local infection, systemic infection, or
both.
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Microorganisms in the bloodstream can cause
lesions in the oral cavity.
Microorganisms causing infection in the lungs
can be transferred to oral tissue and be
present in saliva.
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Infectious Diseases (cont.)


Oral flora may be affected by changes in
salivary flow, administration of antibiotics,
and changes in the immune system.
Opportunistic infection

When an organism that usually is
nonpathogenic causes disease
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Infectious Diseases (cont.)

Microorganisms may penetrate epithelial
surfaces as foreign bodies.

They stimulate the inflammatory response.
• This is a nonspecific response that results in edema
and the accumulation of a large number of white
blood cells.

They stimulate the immune system
• This is a highly specific response that results in the
production of antibodies to the microorganisms that
act as antigens.
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Infectious Diseases (cont.)
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
Humoral immunity (antibodies) is an
effective defense against some
microorganisms.
Cell-mediated immunity is an effective
defense against others such as
intracellular bacteria, viruses, and fungi.
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Bacterial Infections
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Impetigo
Tonsillitis and Pharyngitis
Tuberculosis
Actinomycosis
Syphilis
Necrotizing Ulcerative Gingivitis
Pericoronitis
Acute Osteomyelitis
Chronic Osteomyelitis
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Impetigo
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(pg. 120)
A bacterial skin infection
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Caused by Streptococcus pyogenes and
Staphylococcus aureus
Most commonly involves the skin of the face or
extremities
Usually seen in young children
Requires nonintact skin for infection
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Impetigo (cont.)
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Diagnosis and management



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Lesions are either vesicles or bullae.
The lesions may itch and regional
lymphadenopathy may be present.
The bacteria may be identified from cultures of
the lesion.
Treatment

Topical or systemic antibiotics
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Tonsillitis and Pharyngitis


Inflammatory conditions of the tonsils and
pharyngeal mucosa


(pg. 120)
May be due to many different organisms
Clinical features may include sore throat,
fever, tonsillar hyperplasia, and erythema
of the oropharyngeal mucosa and tonsils.

May be spread by contact with infectious nasal
or oral secretions
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Tonsillitis and Pharyngitis (cont.)

Diagnosis and Management


Laboratory tests can confirm streptococcal
cause.
Group A β (beta)-hemolytic streptococci are
related to scarlet fever and rheumatic fever.
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Scarlet Fever
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Usually occurs in children
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
(pg. 120)
Patients have a fever and a generalized red skin rash
caused by a toxin released by the bacteria.
Oral manifestations in addition to streptococcal
tonsillitis and pharyngitis include


Petechiae on the soft palate
Strawberry tongue
• Fungiform papillae are red and prominent with the dorsal
surface of the tongue exhibiting either a white coating or
erythema.
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Rheumatic Fever
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
A childhood disease that follows a group A
β-hemolytic streptococcal infection


(pg. 120)
Characterized by an inflammatory reaction
involving the heart, joints, and central nervous
system
Heart valve damage may occur.

This may require the patient to be
premedicated prior to dental hygiene
treatment.
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Tuberculosis
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
(pgs. 120-121)
Usually caused by the organism
Mycobacterium tuberculosis

The chief form of the disease is an infection of
the lungs caused by the bacteria.
• The organisms are resistant to destruction by
macrophages.
• After being engulfed, they multiply in the
macrophages and then disseminate in the
bloodstream.
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Tuberculosis (cont.)


(pgs. 120-121)
Signs and symptoms

Include fever, chills, fatigue and malaise,
weight loss, and persistent cough
• Miliary tuberculosis

Involvement of organs such as kidney and liver in
widespread areas of the body
• Scrofula


Involvement of submandibular and cervical lymph
nodes
Oral lesions may occur but they are rare.
• Appear as painful, nonhealing, superficial or deep
slowly enlarging ulcers
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Tuberculosis (cont.)
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Diagnosis of Tuberculosis
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Oral lesions
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Identified by biopsy and microscopic
examination
• Chronic granulomatous lesions with areas of
necrosis surrounded by macrophages,
multinucleated giant cells, and lymphocytes

Tissue
• May be stained to reveal the organisms
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Tuberculosis

Skin test
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An antigen is injected into the skin.
• Purified protein derivative (PPD)
A positive inflammatory reaction occurs if the
person has previously been exposed to the
antigen.
Chest radiographs may be taken after a
positive skin test to see if active disease is
present.
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Tuberculosis (cont.)

An increase has been reported in both in the
number of reported cases and in cases that are
resistant to standard drug regimens.


Tuberculosis incidence has been related to HIV infection
and increased immigration from countries where
tuberculosis is endemic.
It is considered an occupationally transmitted
disease in dentistry.


Standard precautions can prevent transmission.
If the patient has active tuberculosis, treatment can be
deferred.
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Treatment and Prognosis of
Tuberculosis
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
(pg. 121)
Combination medications, including
isoniazid (INH) and rifampin
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
Treatment may continue for months or years.
The patient’s physician should be consulted to
determine whether the patient is infectious.
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Actinomycosis
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
(pgs. 121-122)
An infection caused by a filamentous
bacterium – Actinomyces israelii

Forms abscesses that tend to drain by sinus
tracts
• Sulfur granules


The colonies of organisms appear in pus as tiny,
yellow grains.
The organisms are common, normal
inhabitants of the oral cavity.
• Predisposing factors have not been identified but
infection is often preceded by extraction or an
abrasion of mucosa.
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Actinomycosis (cont.)
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Actinomycosis (cont.)
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Diagnosis
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
Identification of colonies in tissue from the
lesion
Treatment and prognosis

Long-term high doses of antibiotics
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Syphilis
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
(pgs. 122-123)
Caused by a spirochete Treponema
pallidum

Transmitted by direct contact
• The organisms die when exposed to air and changes
in temperature.

Usually transmitted through sexual contact but
may be transmitted through transfusion of
infected blood or to a fetus from an infected
mother
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Syphilis (cont.)
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Syphilis (cont.)
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
(pg. 122) (Table 4-1)
Three stages
Primary stage

The lesion of the primary stage is a chancre
• It forms where the spirochete enters the body.
• It is highly infectious.
• It heals spontaneously and the disease enters a
latent period.
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Syphilis (cont.)
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Syphilis (cont.)
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Secondary stage
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
Diffuse eruptions occur on skin and mucous
membranes
Mucous patches
• Oral lesions that appear as multiple, painless,
grayish white plaques covering ulcerated mucosa
• These lesions are the most infectious.
• They undergo spontaneous remission but may recur
for months or years.
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Syphilis (cont.)
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Tertiary stage


Chiefly involves the cardiovascular system and
the nervous system
Gumma
• A firm mass
• Noninfectious
• A destructive lesion that can result in perforation of
the palatal bone
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Congenital Syphilis


(pg. 122)
Transmitted from an infected mother to the
fetus

May cause serious and irreversible damage
• Facial and dental abnormalities
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Diagnosis and Treatment of
Syphilis
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
Lesions on skin may be identified by darkfield microscopy


(pg. 123)
Blood tests include VDRL and fluorescent
treponemal antibody absorption test (FTAABS)
Treatment

Treated with penicillin
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Necrotizing Ulcerative Gingivitis
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
(pg. 123)
A painful, erythematous gingivitis with
necrosis of interdental papillae


Most likely caused by both a fusiform bacillus
and a spirochete (Borrelia vincentii)
Associated with decreased resistance to
infection
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Necrotizing Ulcerative Gingivitis
(cont.)
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Necrotizing Ulcerative Gingivitis
(cont.)

Diagnosis



Necrosis results in cratering of the interdental
papillae.
Sloughing of necrotic tissue causes a
pseudomembrane over the tissue.
Treatment


Gentle debridement
Antibiotics if fever is present
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Pericoronitis
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
(pg. 123)
Inflammation around the crown of a
partially erupted, impacted tooth


Most commonly a lower third molar
Trauma from an opposing molar and impacted
food under the soft tissue flap (operculum) may
precipitate.
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Diagnosis of Pericoronitis

The tissue around the crown of a partially
erupted tooth is swollen, erythematous,
and painful.
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Treatment and Prognosis of
Pericoronitis
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

Mechanical debridement
Irrigation of the pocket
Systemic antibiotics
Often the long-term solution is removal of
the offending tooth
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Acute Osteomyelitis
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
(pgs. 123-124)
Acute inflammation of the bone and bone
marrow
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
Most commonly the result of a periapical
abscess
May follow fracture of a bone
May result from a bacteremia
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Acute Osteomyelitis (cont.)
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Diagnosis of Acute Osteomyelitis

Diagnosis


Identification of the causative organism is
based on culture results.
Treatment is based on antibiotic sensitivity
testing.
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Treatment and Prognosis of Acute
Osteomyelitis
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

(pg. 123)
Drainage of the area
Appropriate antibiotics
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Chronic Osteomyelitis
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(pgs. 123-124)
A long standing inflammation of bone
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

The involved bone is painful and swollen.
Radiographs reveal a diffuse and irregular
radiolucency that can eventually become
opaque.
Known as chronic sclerosing osteomyelitis
when radiopacity develops
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Chronic Osteomyelitis (cont.)
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Diagnosis of Chronic Osteomyelitis


(pg. 124)
Biopsy results and histologic examination
that show chronic inflammation of bone
and marrow
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Treatment of Chronic
Osteomyelitis
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


(pg. 124)
Debridement
Administration of systemic antibiotics
Some patients may require hyperbaric
treatment.
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Fungal Infections
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

Candidiasis
Deep fungal infections
Mucormycosis
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Candidiasis
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
(pgs. 124-127)
The outcome of an overgrowth of Candida
albicans

This can result from many different conditions.
• Antibiotics, cancer chemotherapy, corticosteroid
therapy, dentures, diabetes mellitus, HIV infection,
hypoparathyroidism, infancy, multiple myeloma,
primary T-lymphocyte deficiency, xerostomia

The organisms can be identified in a scraping
of the lesion.
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Candidiasis (cont.)
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
(pgs. 124-127)
Types
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Pseudomembranous candidiasis
Erythematous candidiasis
Denture stomatitis
Chronic hyperplastic candidiasis
Angular cheilitis
Chronic mucocutaneous candidiasis
Median rhomboid glossitis
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Pseudomembranous
Candidiasis
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
(pg. 125)
A white curdlike material is present on the
mucosal surface.


The mucosa is erythematous underneath.
The patient may complain of a burning
sensation and/or a metallic taste.
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Pseudomembranous Candidiasis
(cont.)
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Erythematous Candidiasis


(pg. 125)
The presenting complaint is an
erythematous, often painful mucosa.

May be localized to one area of oral mucosa or
be more generalized
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Erythematous Candidiasis (cont.)
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Denture Stomatitis
(Chronic Atrophic Candidiasis)


(pgs. 125-126)
The most common type of candidiasis



The mucosa is erythematous, but the change
is limited to the mucosa covered by a full or
partial denture.
The pattern follows the outline of the RPD or
denture.
Usually asymptomatic
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Denture Stomatitis
(Chronic Atrophic Candidiasis) (cont.)
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Chronic Hyperplastic Candidiasis
(Candidal Leukoplakia)


(pgs. 125-126)
A white lesion that does not wipe off the
mucosa


It will respond to antifungal medication.
A lesion that does not respond to antifungal
medication should be biopsied.
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Chronic Hyperplastic Candidiasis
(Candidal Leukoplakia) (cont.)
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Angular Cheilitis


(pg. 126)
Erythema or fissuring at the labial
commissures

Most commonly from Candida, but may be
caused by other factors such as nutritional
deficiency
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Angular Cheilitis (cont.)
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Chronic Mucocutaneous
Candidiasis


(pg. 126)
A severe form that usually occurs in
patients who are severely
immunocompromised

The patient has chronic oral and genital
mucosal candidiasis and skin lesions as well.
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Median Rhomboid Glossitis


(pgs. 126-127)
An erythematous, often rhomboid shaped,
flat to raised area on the midline of the
posterior dorsal tongue


Candida has been identified in some lesions,
and some lesions disappear with antifungal
treatment.
The response is not consistent, though.
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Median Rhomboid Glossitis (cont.)
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Diagnosis and Treatment of
Median Rhomboid Glossitis


(pg. 127)
Diagnosis and treatment



A mucosal smear is obtained and sent to the
laboratory for staining and examination.
In some patients, candidiasis is persistent and
recurrent.
It may be a sign of a severe underlying medical
problem.
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Diagnosis and Treatment of
Median Rhomboid Glossitis (cont.)
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Deep Fungal Infections


(pg. 127)
Oral lesions may be caused by deep
fungal infections such as histoplasmosis,
coccidioidomycosis, blastomycosis, and
cryptococcosis.


They all primarily involve the lungs.
There is a regional distribution of these lesions.
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Diagnosis of Deep Fungal
Infections


(pg. 127)
Made by biopsy and microscopic
examination


Oral lesions are preceded by involvement of
the lungs.
Oral lesions are chronic, nonhealing ulcers that
can resemble squamous cell carcinoma.
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Treatment of Deep Fungal
Infections


(pg. 127)
Systemic antifungal medications such as
amphotericin B, ketoconazole, or
itraconazole

Latent infections may remain following
treatment and reappear if the immune system
becomes deficient.
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Mucormycosis


(pgs. 127-128)
A rare fungal infection



The organism is commonly found in soil and
usually is nonpathogenic.
Infection may occur with diabetic and
debilitated patients.
The disease can present as a proliferating or
destructive mass in the maxilla.
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Viral Infections





Human Papillomavirus Infection
Herpes Simplex Infection
Varicella-Zoster Virus
Epstein-Barr Virus
Coxsackievirus Infections
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Human Papillomavirus Infection




(pgs. 128-129)
Verruca Vulgaris
Condyloma Acuminatum
Focal Epithelial Hyperplasia
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Human Papillomavirus Infection
(cont.)


More than 100 types of human
papillomavirus (HPV) have been identified.


(pg. 128)
Several have been identified in oral lesions
and some in normal oral mucosa.
Also implicated in neoplasia
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Verruca Vulgaris (Common Wart)


(pgs. 128-129)
A papillary oral lesion caused by a
papillomavirus.



Usually transmitted from skin to oral mucosa
Autoinoculation usually occurs through finger
sucking or fingernail biting.
Usually a white, papillary, exophytic lesion that
closely resembles a papilloma
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Verruca Vulgaris
(Common Wart) (cont.)
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Diagnosis of Verruca Vulgaris


(pg. 128)
Biopsy and histologic examination reveal
the light microscopic features of this
lesion.

Immunologic staining may help identify viruses.
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Treatment and Prognosis of
Verruca Vulgaris


Conservative surgical excision


(pg. 129)
Lesion may recur.
Patients with finger lesions should refrain
from finger sucking or fingernail biting to
prevent reinoculation.
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Condyloma Acuminatum


A benign papillary lesion caused by a
papillomavirus




(pg. 129)
Generally transmitted by sexual contact
May be transmitted to the oral cavity through oral-genital
contact or self-inoculation
Papillary, bulbous pink masses that can occur anywhere
in the oral mucosa
• Multiple lesions may be present.
Treatment


Conservative surgical excision
Recurrence is common.
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Condyloma Acuminatum (cont.)
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Focal Epithelial Hyperplasia
(Heck Disease)


(pg. 129)
Characterized by the presence of multiple
whitish to pale pink nodules distributed
throughout oral mucosa



Most common in children
Lesions are generally asymptomatic and do
not require treatment.
Resolve spontaneously within a few weeks
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Focal Epithelial Hyperplasia
(Heck Disease) (cont.)
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Herpes Simplex Infection


There are two major forms of herpes
simplex viruses – type 1 and type 2


(pgs. 129-132)
Oral infections are mostly caused by type 1
and genital infections are most commonly
caused by type 2
Herpes simplex is one of a group of
viruses called human herpes viruses
(HHV).
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Primary Herpetic Gingivostomatitis


The oral disease caused by initial infection with
herpes simplex virus



(pg. 130)
Painful, erythematous, and swollen gingiva and multiple
tiny vesicles on perioral skin, vermilion border of lips,
and oral mucosa may be seen.
• The vesicles progress to form ulcers.
The patient may have systemic symptoms such as fever,
malaise, and cervical lymphadenopathy.
Most commonly occurs in children between 6
months and 6 years of age

The majority of infections are thought to be subclinical.
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83
Primary Herpetic Gingivostomatitis
(cont.)
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84
Recurrent Herpes Simplex
Infection


The virus tends to persist in a latent state.


(pgs. 130-132)
Usually in nerve tissue of the trigeminal
ganglion
It is estimated that one third to one half of
the population in the United States
experiences recurrent herpes simplex
infection.
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Recurrent Herpes Simplex
Infection (cont.)


The most common location for recurrent
infection is on the lips – herpes labialis.


(pg. 130)
Also called a cold sore or fever blister
Episodes may be stimulated by stress.

May be sunlight, menstruation, fatigue, fever,
and emotional stress
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Recurrent Herpes Simplex
Infection (cont.)
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Recurrent Herpes Simplex
Infection (cont.)


Occurs intraorally on keratinized mucosa
that is attached to bone


(pgs. 130-131)
Painful groups of small vesicles that ulcerate
and coalesce to form a single ulcer with an
irregular border
The patient may have a prodrome with
symptoms such as pain, burning, or
tingling.
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Recurrent Herpes Simplex
Infection (cont.)
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Recurrent Herpes Simplex
Infection (cont.)


Transmitted by direct contact with an infected
individual



The primary infection occurs at the site of
inoculation.
The amount of virus is highest in the vesicle stage.
Herpetic whitlow


(pgs. 130-132)
A painful infection of the fingers due to a primary
or secondary infection
Herpes simplex can also cause an eye
infection.
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Recurrent Herpes Simplex
Infection (cont.)
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91
Diagnosis of Recurrent Herpes
Simplex Infection (Cont.)
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92
Diagnosis of Recurrent Herpes
Simplex Infection (Cont.)


(pgs. 131-133) (Table 4-2)
Generally based on clinical appearance

Changes in epithelial cells can be seen
microscopically.
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Diagnosis of Recurrent Herpes
Simplex Infection (cont.)
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Treatment of Recurrent Herpes
Simplex Infection


(pg. 132)
Antiviral drugs where appropriate

These drugs have not been shown to be
consistency effective in treating lesions except
in immunocompromised patients.
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Varicella-Zoster Virus


(pgs. 132-134)
Causes both chickenpox (varicella) and
herpes zoster (shingles)

Respiratory aerosols and contact with
secretions from skin lesions transmit the virus.
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Chickenpox


A highly contagious disease



(pgs. 132-133)
Causes vesicular and pustular eruptions of
skin and mucous membranes
Systemic symptoms include headache, fever,
and malaise.
Usually occurs in children
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Chickenpox (cont.)
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Herpes Zoster
(Shingles)


Secondary chickenpox in an adult




(pgs. 133-134)
Characterized by a unilateral, painful eruption of vesicles
along the distribution of a sensory nerve
Any branch of the trigeminal nerve may be
involved if lesions affect the face.
Vesicles are often preceded by pain, burning, or
paresthesia.
The disease usually lasts for several weeks.

Neuralgia may take months to resolve.
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Herpes Zoster
(Shingles) (cont.)
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100
Herpes Zoster
(Shingles) (cont.)
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Diagnosis of Varicella Zoster


(pg. 134)
Generally made based on clinical features

Biopsy or smear may show the same type of
virally altered epithelial cells seen in herpes
simplex infection.
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Treatment of Varicella Zoster


(pg. 134)
Varicella generally is treated with
supportive care.

Antiviral drugs may be used for
immunocompromised patients and for patients
with herpes zoster.
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Epstein-Barr Virus Infection


(pgs. 134-135)
Implicated in several diseases, including
infectious mononucleosis, nasopharyngeal
carcinoma, Burkitt lymphoma, and hairy
leukoplakia
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Infectious Mononucleosis


Characterized by sore throat, fever,
generalized lymphadenopathy, enlarged
spleen, malaise, and fatigue


(pgs. 134-135)
Petechiae may appear on the palate.
In the United States, infectious
mononucleosis occurs primarily among
adolescents and young adults.

Often transmitted by kissing
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Hairy Leukoplakia


(pg. 135)
An irregular, corrugated, white lesion most
commonly occurring on the lateral border
of the tongue


Epstein-Barr virus (EBV) is considered to be
the cause of the lesion.
It occurs most commonly in patients infected
with HIV but has also been reported in patients
who are not infected with HIV.
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Hairy Leukoplakia (cont.)
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Coxsackievirus Infections


Causes several different infectious
diseases


(pg. 135)
May be transmitted by fecal-oral
contamination, saliva, and respiratory droplets
Three have distinctive oral lesions



Herpangina
Hand-foot-and-mouth disease
Acute lymphonodular pharyngitis
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Herpangina


Characterized by fever, malaise, sore
throat, and difficult swallowing (dysphagia)



(pg. 135)
Includes vesicles on the soft palate
Erythematous pharyngitis
Resolves in less than 1 week without
treatment.
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Herpangina (cont.)
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Hand-Foot-and-Mouth Disease

Usually occurs in epidemics in children
less than 5 years old



Multiple macules or papules occur on the skin,
typically on feet, toes, hands, and fingers.
Oral lesions are painful vesicles that can occur
anywhere in the mouth.
Resolves within 2 weeks
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Diagnosis and Treatment of HandFoot-and-Mouth Disease


Diagnosis


(pg. 135)
The distribution of skin lesions and mild
systemic symptoms help differentiate the
condition from herpes simplex infection.
Treatment

Generally not required
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Acute Lymphonodular Pharyngitis


Characterized by fever, sore throat, and
mild headache


(pg. 135)
Hyperplastic lymphoid tissue of the soft palate
or tonsillar pillars appears as yellowish or dark
pink nodules.
Lasts several days to 2 weeks and does
not usually require treatment
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Other Viral Infections That May
Have Oral Manifestations


Measles




(pgs. 135-136)
Caused by a type of virus called a
paramyxovirus
A highly contagious disease causing systemic
symptoms and a skin rash
Koplik spots may occur in the oral cavity.
• They are small erythematous macules.
Mumps


A viral infection of the salivary glands
Most commonly causes bilateral swelling of the
parotid glands
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Human Immunodeficiency Virus (HIV) and
Acquired Immunodeficiency Syndrome (AIDS)


The virus is transmitted by




(pg. 136)
Sexual contact with an infected person
Contact with infected blood and blood products
Infected mothers to their infants
Infects cells of the immune system,
particularly CD4 T-helper lymphocytes

This lymphocyte participates in cell-mediated
immunity and in regulating the immune
response.
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The Spectrum of HIV


(pg. 136)
Many individuals experience an acute
disease shortly after infection with HIV, but
others are asymptomatic.


Infected individuals may not have any signs or
symptoms of disease for some time, but in
most patients a progressive immunodeficiency
develops.
As the immune system becomes deficient, lifethreatening opportunistic infections and
cancers occur.
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Diagnosing AIDS


(pgs. 136-137) (Box 4-1)
The current definition includes HIV
infection with severe CD4 lymphocyte
depletion.


< 200 CD4 lymphocytes per microliter of blood
Normal level is between 550 and 1000
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HIV Testing


(pg. 136)
Two antibody tests are used to determine
if a person is infected.


ELISA (enzyme-linked immunosorbent assay)
is used first.
When this test is positive twice, it is followed by
the Western blot test.
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Clinical Manifestations of AIDS


An initial infection may be asymptomatic.



(pgs. 136-137)
Some people may develop lymphadenopathy.
Others may develop an acute illness
resembling mononucleosis.
Following an acute illness, some
individuals may have persistent
lymphadenopathy.

Many become completely asymptomatic.
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Clinical Manifestations of AIDS
(cont.)

The virus infects cells of the immune
system.


In time, the immune system becomes deficient.
AIDS-related complex is the occurrence of
several signs and symptoms together.

These may include oral candidiasis, fatigue,
weight loss, and lymphadenopathy.
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Clinical Manifestations of AIDS

Antibodies to HIV usually begin to become
detectable about 6 weeks following
infection.


In some people, antibodies may not be
detectable for 6 months or up to a year or
longer.
This is called the “window of infectivity.”
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Clinical Manifestations of AIDS
(cont.)


(pg. 137-138)
The spectrum of HIV infection includes
everything from an asymptomatic infection
to “full blown” AIDS.


HIV
• Human immunodeficiency virus
AIDS
• Acquired immunodeficiency syndrome
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Clinical Manifestations of AIDS
(cont.)
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Medical Management of AIDS


Tests such as PCR are used to measure
the amount of HIV circulating in serum.



(pg. 137)
The measured amount is called the viral load.
Measurement of the viral load along with
the CD4 lymphocyte count is used to
assess HIV infection.
Patients are managed with combinations
of antiretroviral drugs and drugs used to
treat opportunistic infections.
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Oral Manifestations of AIDS (cont.)


Many oral lesions are associated with
patients with HIV infection and AIDS.


(pgs. 137-138) (Box 4-2)
Some lesions indicate developing
immunodeficiency and predict AIDS in patients
who are HIV positive.
Oral lesions develop due to deficiency in
CMI and depletion of T-helper cells.

Oral lesions include opportunistic infections,
tumors, and autoimmune-like diseases.
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Oral Manifestations of AIDS (cont.)













(pgs. 138-142) (Box 4-2)
Oral candidiasis
Herpes simplex infection
Herpes zoster
Hairy leukoplakia
Human papillomavirus (HPV) infections
Kaposi sarcoma
Lymphoma
Gingival and periodontal disease
Spontaneous gingival bleeding
Aphthous ulcers
Salivary gland disease
Mucosal melanin pigmentation
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Oral Candidiasis (Thrush)


All different types may occur.



(pgs. 138-139)
Topical and systemic antifungal treatment may
be used.
Recurrence is common.
In HIV-positive patients, it generally signals
the beginning of progressively severe
immunodeficiency.
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Oral Candidiasis (Thrush) (cont.)
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Herpes Simplex Infection



(pgs. 138-139)
When the immune system becomes
deficient the infection appears as
persistent, superficial, painful ulcers that
may be located anywhere in the oral
cavity.
An ulceration due to herpes simplex that
has been present for more than 1 month
“meets the criteria for the diagnosis of
AIDS.”
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Herpes Simplex Infection (cont.)
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Herpes Zoster


(pg. 139)
Generally follows the usual pattern when it
occurs in a person who is HIV positive


In the facial and oral area, the lesions follow
branches of the trigeminal nerve.
It is a sign of developing immunodeficiency.
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Hairy Leukoplakia


Caused by Epstein-Barr virus



Most cases are an oral manifestation of HIV virus, but it
is not always the case
It almost always occurs on the lateral borders of
the tongue, where it appears as an irregular, white
lesion with a corrugated surface.
Chronic tongue chewing and hyperplastic
candidiasis can resemble the lesion.


(pg. 139)
EBV is the most reliable method of diagnosis
Treatment


Generally, it is not treated
It is a predictor of AIDS in HIV-positive individuals.
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Hairy Leukoplakia (cont.)
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Human Papillomavirus Infections
(HPV)


Papillary oral lesions from several different
papillomaviruses have been described in
persons with HIV infection.



(pgs. 139-140)
May have normal color or be erythematous
May be persistent and occur in multiple oral
locations
May be associated with antiretroviral
treatment
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Human Papillomavirus Infections
(HPV) (cont.)
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Kaposi Sarcoma


An opportunistic neoplasm that may occur in
patients with HIV infection.



Oral lesions appear as reddish-purple, flat or raised
lesions
May be seen anywhere in the oral cavity, most
commonly on the palate and gingiva
Diagnosis


(pg. 140)
Biopsy
Treatment

Surgical excision, radiation treatment, chemotherapy
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Kaposi Sarcoma (cont.)
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Lymphoma


A malignant tumor that may occur in
association with HIV infection.



Appears as a nonulcerated, necrotic, or
ulcerated mass
May be surfaced by ulcerated or normalcolored erythematous mucosa
Diagnosis


(pgs. 140-141)
Biopsy and histologic examination
Treatment

Chemotherapeutic drugs
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Lymphoma (cont.)
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Gingival and Periodontal Disease


(pg. 141)
Unusual forms of gingival and periodontal
disease may develop


Linear gingival erythema (LGE)
Necrotizing ulcerative periodontitis (NUP)
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Gingival and Periodontal Disease
(cont.)
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Linear Gingival Erythema (LGE)


Three characteristic features




(pg. 141)
Spontaneous bleeding
Punctate or petechiae-like lesions on attached
gingiva and alveolar mucosa
A bandlike erythema of the gingiva that does
not respond to therapy
LGE occurs independently of oral hygiene
status.
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Necrotizing Ulcerative Periodontitis
(NUP)


(pg. 141)
Characterized by intense erythema and
extremely rapid bone loss

Necrotizing stomatitis
• Extensive focal areas of bone loss along with
features of NUP
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Gingival and Periodontal Disease

Treatment


Scaling, root planing, soft tissue curettage
Intrasulcular lavage, chlorhexidine mouthrinse,
systemic metronidazole
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Spontaneous Gingival Bleeding


(pg. 142)
A decrease in platelets may occasionally
be seen in patients with HIV.


Due to an autoimmune type of
thrombocytopenic purpura
In these patients, “a platelet count and
bleeding time should be considered before
deep scaling procedures.”
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Aphthous Ulcers


(pg. 142)
There appears to be an increase in the
number of these ulcers in patients with HIV
infection.


Ulcers resembling major aphthous ulcers
appear as deep, persistent, painful ulcers.
They respond to steroids.
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Aphthous Ulcers (cont.)
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147
Salivary Gland Disease


(pg. 142)
Bilateral parotid gland enlargement may
occur in patients who are HIV positive.

May be related to medication or salivary gland
disease
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Salivary Gland Disease (cont.)
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Mucosal Melanin Pigmentation


(pg. 142)
Macular areas of melanin pigmentation
may occur in patients with HIV infection.

The cause is unclear.
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Discussion Questions






What is impetigo?
What organism causes syphilis?
What are the different forms of Candida?
What is a wart?
What causes mononucleosis?
What is the difference between HIV and AIDS?
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