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Oral lesions and HIV
Praxis – Fortbildung
ORAL LESIONS AND HIV
An approach to the diagnosis of oral mucosal lesions for the dentist in private practice
CESAR A. MIGLIORATI* and ERICA K. J. MIGLIORATI**
*Klinik für Alters- und Behindertenzahnmedizin, Zürich (bis 1996)
**Privatpraktikerin, São Paulo
(Deutscher Text siehe Seite 869)
(Texte français voir page 871)
The diagnosis and treatment of oral mucosal lesions in HIV infected individuals is of importance. Oral lesions are reliable indicators of HIV infection and immunosuppression. They are
important for staging HIV disease, they have been used as clinical markers in trials to test
drug efficacy, and to determine the correct time for institution of treatment for HIV or prophylaxis against opportunistic infections. For the patients, they can cause pain, loss of taste
and severe discomfort, leading to decreased quality of life. In more severe cases, they can
disseminate and become life-threatening.
Several types of lesions may affect the oral mucosa of HIV infected individuals. Although
caused by different etiological agents, these lesions may have similar clinical appearance.
They may also look like other oral mucosal lesions not commonly associated with HIV infection. Their correct diagnosis is important so adequate treatment can be prescribed. This article provides information to the dentist in private practice on how to elaborate a differential
diagnosis and arrive to a final diagnosis of oral mucosal lesions in HIV infected individuals.
Key words: differential diagnosis, HIV, oral diagnosis, oral lesions, oral medicine
Introduction
▲
The dentist in private practice as part of the team of primary care providers, will have to care for an increasing
number of HIV infected patients (MERSON 1993). In addition to dental and periodontal problems common to all
individuals and to severe medical complications, HIV infected patients may develop several oral mucosal lesions
and diseases (SCULLY et al. 1991 a, b, EC-CLEARINGHOUSE
1993). In HIV infected patients, these oral mucosal lesions
HIV positive man with oral candidiasis. Note the
white colonies of fungi on the dorsal surface of the
tongue. These lesions can be scraped off with gaze.
Address for correspondence:
Cesar A. Migliorati, D. D. S., M. S. – Oral Medicine
Specialist, American Board of Oral Medicine. Damianstrasse 7, CH-5430 Wettingen, Switzerland.
may have a unique clinical presentation and may not respond to the treatment in the usual manner (JONES et al.
1992, GROSSMAN et al. 1993). Physicians and dentists do
not receive sufficient training in diagnosing and managing oral mucosal diseases and lesions. Thus, such problems may go undiagnosed and untreated for weeks or
months, leading to decreased quality of life for the patients.
In order to diagnose an oral mucosal lesion in an HIV infected patient, as for in any other patient, the dentist must
use a systematic approach (Fig. 1). This includes taking a
complete review of the history of the lesion, taking a review of the medical, dental and social history, and listing
all medications being used. Following, a thourough extraoral and intraoral examination should be performed. All
abnormal findings should be evaluated and recorded. With
the analysis of the data collected, the dentist has the possibility of building a differential diagnosis. Differential diagnosis is the grouping of all possible lesions or diseases
that would have a similar history and clinical presentation
with the present illness (WOOD & GOAZ 1991). The most
probable and dangerous alternatives should be ruled out
first.
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White lesions
Oral mucosal lesion
After the differential diagnosis is determined, the dentist
can start testing all possibilities by using the appropriate
diagnostic tests indicated for that particular lesion or disease. For example, if the first possibility on the list of differential diagnosis is oral candidiasis, a culture or a smear
for fungal identification can be taken. If the clinical impression is that of a cancerous lesion, a biopsy should be
taken immediately. When the first possibility on the list of
differential diagnosis is ruled out, the next possibility
should be tested. This procedure should lead the dentist to
the correct diagnosis of the lesion, after which the appropriate therapy can be instituted.
The objective of this article is to discuss the differential
diagnosis of common lesions affecting the oral mucosa of
HIV infected individuals. Two different group of lesions
will be discussed: white lesions and oral ulcerations.
Mucosal white lesions are frequently observed during routine oral examination of HIV infected individuals. The
two most important and common are candidiasis, a fungal infection, and hairy leukoplakia (HL), a viral infection
(SILVERMAN et al. 1986, GREENSPAN et al. 1987, GRASSI et
al. 1991). Candidiasis is an infection clinically represented by an overgrowth of the Candida species. The fungus attaches and proliferates on the epithelial surface,
forming white creamy colonies easely observed clinically.
In chronic infections the microorganisms may penetrate
deep in the tissues, causing a thickening of the epithelium
and the formation of surface keratin (Candidal leukoplakia). White lesions of oral candidiasis in HIV infected
patients can occur on the palate, on the buccal mucosa, on
the oropharynx and on the lateral borders of the tongue.
On the other hand, the white appearance of HL results
from the thickening of the keratin layer in response to the
infection of the oral epithelial cells by Epstein Barr virus
(EBV). Hairy leukoplakia affects mostly the lateral borders of the tongue. Therefore, the white appearance and
the location can make oral candidiasis and HL look clinically alike. However, one is caused by a fungus and the
other by a virus. The simple act of scraping the surface of
a white lesion will remove candida colonies but will not
remove HL, giving the clinician important information
about the possible etiology.
Therefore, when examing an HIV infected patient with
white lesions on the oral mucous membrane, oral candidiasis and hairy leukoplakia should always be included
in the differential diagnosis. A final diagnosis can be made
by evaluating the history of the two lesions, by examining clinical appearence, location and symptoms. Oral candidiasis is usually symptomatic and may cause pain, burning sensation and lack of appetite. HL is usually asymptomatic. The appropriate laboratory tests help to confirm
the diagnosis. Oral candidiasis is diagnosed by culture and
hairy leukoplakia by biopsy. These two lesions are important markers of HIV infection. They usually indicate
presence of immunosuppression, and require different
therapeutic approach.
Candidiasis can be treated with antifungal medication.
Because of frequent recurrent episodes of oral candidiasis in HIV infected individuals, a prevention protocol may
be necessary for certain patients. Therefore, impeccable
oral hygiene should be maintained and supportive treatment with topical antifungals and mouth rinses may be indicated. Hairy leukoplakia does not require any treatment.
Fig. 2.1 Pseudomembranous candidiasis of the palate.
Lesions can be removed by scraping. The patient has lost
the appetite and the taste of food.
Fig. 2.2 Oral candidiasis of the lateral border of the
tongue. Lesions can not be removed by scraping and are
painful. Note similarity with hairy leukoplakia.
History of the
lesion
Medical
history
Dental and
social history
Extra and intraoral examination
Collection of signs and symptoms
Differential
diagnosis
Clinical and laboratorial
tests
Final diagnosis
Therapy
Follow-up
Fig. 1 Systematic approach to the diagnosis of oral
mucosal lesions
862
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Oral lesions and HIV
Fig. 2.3 Hairy leukoplakia of the lateral border of the
tongue. Lesion can not be removed by scraping and is
asymptomatic.
Fig. 2.4 Hairy leukoplakia affecting the lateral border
of the tongue and the right buccal mucosa. The culture
of this lesion was negative for candida species.
Fig. 2.5 Tobacco
induced
leukoplakia.
The
histopathological examination showed mild epithelial
dysplasia and absence of candida organisms. The patient is HIV negative.
Fig. 2.6 Classical red and white atrophic lesions of
lichen planus affecting the dorsum of the tongue. The
patient was complaining of pain and tested negative for
oral candidiasis and HIV.
Fig. 2.7 and 2.8 Note the similarity of these two lesions affecting the buccal mucosa. The patient in figure 2.7 has
white sponge nevus, an autosomic dominant condition, is asymptomatic and is HIV negative. The patient in figure 2.8
has oral candidiasis, complained of burning sensation and is HIV positive.
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There are no reports suggesting dissemination of EBV
from the oral lesions to other parts of the body. It is also
possible that oral candidiasis and hairy leukoplakia appear
sumultaneously.
A clinician must be able to recognize oral candidiasis and
HL, differentiate them from one another, and from other
white lesions that can affect the general population or the
HIV infected individual. Some of these include lichen
planus, white sponge nevus, leukoedema, and the precancerous leukoplakia and erythroleukoplakia.
It is important to consider that on occasion, these oral
manifestations may have some red component as in the
case of precancerous erythroleukoplakia or in lichen
planus, or may be completely red like in the case of erythematous candidiasis. In the latter case, the lesion cannot
be scraped off the surface.
One should also keep in mind that not all patients with
white lesions in the mouth are HIV infected. On the other
hand, not all white lesions in the oral mucosa of HIV infected patients are candidiasis or hairy leukoplakia. Thus,
Table I Differential diagnosis of candidiasis, hairy leukoplakia and other white or white and red oral mucosal
lesions in HIV infected patients
Lesions
Features
Candidiasis
Hairy Leukoplakia Precancerous
Lichen Planus
Leukoplakia or
Erythroleukoplakia
White Sponge
Nevus
Leukoedema
Symptoms
Pain, loss of taste,
distortion of taste,
burning, discomfort
Asymptomatic
Asymptomatic or
painful
Pain, discomfort,
burning when eating
Asymptomatic,
mild roughness of
mucosa
Asymptomatic
Clinical
presentation
and location
Pseudomembranous: White or
creamy colonies
that scrape off
Erythematous:
Redness of palate,
tongue, gingiva,
oral mucosa in
general
Hyperplastic:
White plaques that
do not scrape off
Angular cheilitis:
White and red
cracks of the corners of the lips
White plaques with
flat or corrugated
surface on the lateral borders of the
tongue that do not
scrape off.
Occasionally present on other areas
of the mouth
White plaques and
red changes of the
mucosa, that do not
scrape off.
Can be present anywhere in the mouth.
Frequent areas are
buccal mucosa, lateral borders of the
tongue, floor of the
mouth and gingiva
White striations or
plaques that do not
scrape off. Lesions
may also be red and
ulcerated. Frequently observed on
buccal mucosa,
tongue and gingiva
White lesions with
rough, wrinkled surface, that occur
mostly on the buccal mucosa or may
sometimes be
widespread, affecting the entire oral
mucosa. Does not
scrape off
Gray-white, diffuse,
filmy, milky opalescence of the buccal
mucosa.
Occasional wrinkling or corrugation
may be seen. Does
not scrape off
Etiology
Fungus
(Candida sp.)
Herpes Virus
(Epstein Barr)
Unknown. May be
accociated with
tobacco, alcohol
Unknown
Autosomal dominant transmitted
condition
Unknown. Possible
abnormal mastication
Adults, chronic, frePatient
population and quent recurrences in
characteristics HIV patients
Almost exclusively
in HIV patients
Adults, over 45
years of age, most
of times smokers.
Rare in HIV
Over 50, 60%
women, various
clinical patterns.
Uncommon in HIV
Appears early in
life, typically before
puberty. Rare in
HIV
Racial clustering
amongst blacks
mostly. May be seen
in HIV
Diagnosis
Culture,
histopathology
Histopathology
Histopathology
Histopathology
Histopathology
Clinical,
histopathology
Treatment
Systemic: Fluconazole, Ketoconazole,
Itraconazole
Topical: Nystatin,
Miconazole
None. In severe
cases: Acyclovir
Surgery. Partial excision or complete
excision. Experimental therapy with
vitamin A analogues/ß Carotene
Severe: systemic
steroids
Mild to moderate:
topical steroids
No treatment
No treatment
None
Decrease tobacco
and alcohol; eliminate all irritants
Topical steroids,
good oral hygiene
None
None
Persistant until late
stages of HIV disease
May progress into
squamous cell cancer. Frequent follow-up necessary
Chronic, recurrences likely. Ulcerated lesions may
have premalignant
potential. Candidiasis may be part of
lesion
Good prognosis,
benign nature
Good prognosis,
benign nature
Mouth rinses
Prophylaxis
and prevention (Chlorhexidine),
of recurrences Nystatin, Miconazole
Prognosis
864
Frequent recurrences second to
immunosuppression
and resistance to
treatment
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Oral lesions and HIV
Fig. 2.9 Painful recurrent aphtha ulcer affecting the
soft palate and uvula. Note that the ulcer is next to several bluish-purple lesions of Kaposi’s sarcoma.
Fig. 2.10 Painful nonspecific ulcer that appeared on
the lingual aspect of the retromolar area after the extraction of the first and second mandibular molars.
Fig. 2.11 Traumatic palantal ulcer caused by a fractured removable prosthesis.
Fig. 2.12 Painful ulcerative lesion on the lateral border of the tongue present for four months. The
histopathologic examination confirmed invasive squamous cell carcinoma. The patient smoked two to three
packs of cigarets daily.
Fig. 2.13 Painful ulcers on the palatal aspect of the
maxillary first molar caused by the Herpes simples virus.
Ulcers are located on keratinized oral mucosa.
Fig. 2.14 This patient complained of severe pain on
the palatal gingiva, present for several days. Observe ulceration and necrosis of the gingival surface and palate.
The differential diagnosis included necrotizing gingivitis, herpes and bacterial infection. The culture was positive for E. coli and Candida sp. The patient was treated
with a combination of antibiotic and antifungal medication.
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Table II
Differential diagnosis of oral ulcerations in HIV infected patients
Lesions
Features
Aphthas ulcer
nonspecific ulcer
Squamous cell
carcinoma
Primary or recurrent
Herpes simples
Cytomegalovirus
Syphilis
Other bacterial
infections
Symptoms
Pain, discomfort
Pain, discomfort.
May also be
asymptomatic
Pain, discomfort
Pain, dysphagia,
odynophagia
Painless
Pain, discomfort
Clinical
presentation
and location
Ulcerations of various sizes, covered
by pseudomembrane and surrounded by erythema. Mostly located in nonkeratinized areas like
soft palate, oropharynx, labial mucosa,
buccal mucosa and
lateral tongue.
Lymphadenopathy
may be present
Single ulcer with
elevated and indurated borders.
Common location
includes the lateral
borders of the
tongue, lips, floor
of the mouth and
gingiva. Metastatic
lymphnodes may
be present
Primary: lip and
gingival involvement by blisters and
ulcers, severe erythema and occasional gingival
bleeding. Fever,
malaise and lymphadenopathy.
Recurrent: blisters
and ulcers mostly
on keratinized epithelium of attached
gingiva, hard palate,
dorsal tongue and
lip
Ulceration that may
appear anywhere in
the oral cavity and
may become extensive. Have been observed on the
tongue, gingiva,
palate and can affect
bone. Oropharynx
and oesophageal ulcers have been described.
Primary: indurated
ulcer with rolled
borders at the site of
innoclation. Heals
within 3 to 12
weeks Lymphadenopathy may
be present
Secondary: mucosal ulcers covered
by pseudomembrane. May persist
up to 8 weeks. Lymphadenopathy may
be present
Ulcers that may be
lacated anywhere in
the oral mucosa.
May be flat or deep
with some induration. Have been observed on the
tongue, palate and
gingiva
Etiology
Unknown. Herpetic Unknown. Tobacco
(Cytomegalovirus,
and alcohol play a
Herpes Zoster
role
virus)? Immunosuppression?
Herpes simples
virus
Herpes virus group
– Cytomegalovirus
Spirochete Treponema pallidum
Gastrointestinal
bacteria, Mycobacterium tuberculosis
Characteristics
Recurrences. On
occasion, unresponsive to treatment
Rare in HIV infected patients
Recurrence. Lesions
may persist for
many weeks or
months. May disseminate
Ulcers may be extensive and disseminate
Oral cavity may
present first or only
lesion
Diagnosis may be
difficult
Diagnosis
History, clinical
presentation and
elimination of other
causes
Biopsy
History, clinical
presentation and
cultur
Biopsy and DNA
probe
History, serologic
tests, darkfield examination of material from active lesion
Culture
Treatment
Systemic and topic
corticosteroid
Surgery, radiation
therapy
Acyclovir
Ganciclovir,
Foscarnet
Penicillin
Antibiogram and
specific antibiotics
Prophylaxis
and prevention
of recurrences
None
Quit smoking and
alcohol consumption. Frequent follow up
Acyclovir may be
used in presence of
frequent recurrence
None
Sexual counseling,
use of barries,
avoidance of
promiscuity
None
Prognosis
Usually good, but
Poor when not
frequent recurrences diagnosed early
may occur
Recurrences may
increase with advanced immunosuppression
Life threatening
upon dissemination
Good, by early
diagnose. May
progress to neurosyphilis
Good.
Poor for
tuberculosis
it is important to take a systematic diagnostic approach
during the examination of all lesions independent of the
HIV status.
Oral Ulcerations
Oral ulcerations can be a common finding during the examination of an HIV infected patient (MACPHAIL et al.
1992). Because ulcers in the oral mucosa are painful, they
may be the reason for consultation with the dentist. Ulcers
may result from infection, inflammation, trauma, malignancy, or be of nonspecific etiology (SILVERMAN et al.
1986, REYES-TERAN et al. 1992, JONES et al. 1992). A correct diagnosis is the basis for adequate treatment and prevention of systemic dissemination in case of infectious eti866
Schweiz Monatsschr Zahnmed, Vol. 107: 10/1997
ology (JONES et al. 1992). Making the correct diagnosis is
also important because of the transmissibility potential
that some of these lesions have like syphilis and herpes.
Whenever an ulcerative lesion is found in the mouth of an
HIV infected patient, the dentist must consider the possibility of infectious disease. Ulcerative lesions caused by
the Herpes virus often affect the oral mucosa (EVERSOLE
1992, SCULLY 1992). Among the herpetic lesions, those
caused by Herpes simples virus are the most common. Although the duration of these herpetic ulcerations may be
the same as observed in the immunocompetent individuals, in many instances the ulcers may persist for several
weeks, may extend to non keratinized oral mucosa, and
may cause severe morbidity for the patients (SILVERMAN
1989, FLAITZ et al. 1996).
Oral lesions and HIV
Fig. 2.15 A 28 year old patient with severe pain in several areas of the oral cavity. Note several ulcerative lesions affecting the palatal mucosa. The patient tested
positive for syphilis and was referred to the physician for
treatment.
Fig. 2.16 Large fungating and painful ulcer on the
alveolar border of the maxilla appeared after the extraction of the pre-molars. The histopathologic examination was positive for Herpes simples virus, Cytomegalovirus and Histoplasmosis (a deep fungal infection). The patient died of disseminated Cytomegalovirus
infection two months later.
Other herpetic infections like Herpes Zoster virus and Cytomegalovirus can also cause ulcerations on the oral cavity (JONES et al. 1992, JONES et al. 1993, HEINIC et al. 1993,
FLAITZ et al. 1996). Lesions caused by Cytomegalovirus
may be extensive and may affect the oropharynx and oesophagus, causing severe pain during deglutition. These
lesions may initiate in the oral cavity and disseminate systemically, becoming lifethreatening. Patients should be
referred immediately for medical care. The diagnosis of
viral lesions can be made by histopathology and microbiological culture.
Another common type of oral ulceration is recurrent aphthous ulcer (MACPHAIL et al. 1992). A patient may have a
solitary lesion or lesions in several areas of the oral mucosa. The main clinical characteristic of this type of lesion
is that it mostly occurs on non keratinized mucosa like the
labial mucosa, buccal mucosa, floor of the mouth and soft
palate. In contrast, herpetic lesions are usually located on
keratinized areas like the lips, the hard palate and the attached gingiva. Aphthae may be a result of trauma, systemic medication, leukopenia, or have nonspecific cause.
They may reccur with frequency. The diagnosis is usually
clinical.
Furthermore, whenever a non healing isolated ulcer is detected, the dentist must consider the possibility of malignancy. Squamous cell carcinoma is the most likely. When
a malignancy is suspected, this possibility should be assessed first. A biopsy is the most indicated diagnostic procedure. Deep fungal infections and bacterial infections
may also present clinically as ulcerative lesions.
mucosal lesion can be reactive, inflammatory, infectious,
or malignant. It can be a localized process or part of a systemic disease.
From the analysis of the data collected during clinical examination, the dentist can construct a list of differential
diagnoses, listing the most probable diseases that could
cause that particular lesion. This procedure should lead to
the final diagnosis of the disease and indicate the most appropriate treatment.
Not uncommonly, oral lesions in HIV patients can cause
severe impairment of oral functions as well as pain and
discomfort. In addition, they are a manifestation of opportunistic diseases second to systemic immunosuppression. Therefore, from the oral cavity they may disseminate systemically and cause a much more dangerous threat
to the patient’s health. Some of the lesions may be transmissible and patients must be counseled on prevention of
transmission (ex: herpes, syphilis, tuberculosis).
The early diagnosis of oral lesions might lead the dentist
to the recognition of a patient who is infected by HIV and
is not aware of it. Thus, the recognition of these lesions is
important for early referral of patients for medical care
and counseling. When the dentist does not feel comfortable in diagnosing and treating oral lesions, a referral to
an Oral Medecine specialist is warranted. The patient
should be informed about the problem and explained
about the reason for referral. By following these guidelines, the dentist will improve the quality of care provided
to HIV infected individuals. The same rationale applies
for all other dental patients bearing an oral mucosal lesion.
Concluding remarks
Literatur
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complete oral examination, the dentist will be able to diagnose oral lesions in patients with HIV disease. Rather
than trying to guess the correct diagnosis, the good diagnostitian should obtain the history of the lesion, should
evaluate signs and symptoms and should determine the
possible etiology. Important factors to be considered in the
differential diagnosis are the history of the lesions, the
clinical appearance, location and symptoms like pain,
burning sensation, and discomfort upon deglution. It is
also important to consider the nature of the lesion. An oral
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Orale Schleimhautveränderungen und HIV
ORALE SCHLEIMHAUTVERÄNDERUNGEN
UND HIV
Eine Übersicht der Differentialdiagnose für den Zahnarzt in der Privatpraxis
CESAR A. MIGLIORATI und ERICA K. J. MIGLIORATI
(Deutsche Kurzfassung von Thomas Vauthier)
(Literatur, Tabellen und Abbildungen siehe englischer Text S. 861–868)
Im Rahmen der zahnärztlichen Tätigkeit muss der möglichst frühzeitigen Abklärung und gegebenenfalls Behandlung oraler Läsionen höchste Bedeutung zukommen. Dies gilt ganz besonders bei HIV-infizierten Patienten, weil allfällige Veränderungen der oralen Schleimhäute
Aufschluss nicht nur über den Verlauf oder das Stadium der HIV-Infektion, sondern auch über
den Grad der Immunodefizienz geben können. Damit kann sich der Patient im Hinblick auf
seine HIV-Erkrankung und eventueller opportunistischer Begleitfunktionen rechtzeitig behandeln lassen.
Der privat praktizierende Zahnarzt steht durch seine diagnostische Tätigkeit in der Mundhöhle an vorderster Front
bei der Entdeckung und Abklärung verschiedener systemischer Erkrankungen mit allfälligen oralen Auswirkungen. Dazu gehören auch Infektionen durch HIV, weil die
virale Immunschwäche in vielen Fällen durch recht spezifische, oder gar pathognomonische orale Schleimhautveränderungen begleitet sein kann. Gerade deswegen
muss vom Privatpraktiker ein Höchstmass an diagnostischem Spürsinn und stomatologischem Wissen gefordert
werden, um nicht Gefahr zu laufen, derartige Läsionen unerkannt, und somit unbehandelt, zu lassen. Grundsätzlich
ist in allen Fällen der Feststellung oraler Schleimhautveränderungen ein Schema sequentieller Massnahmen zur
präzisen Diagnose einzuhalten (Fig. 1). Dazu gehören zuerst eine umfassende Anamnese (nicht nur zahnmedizinisch und betreffend die vorhandene Läsion, sondern auch
allgemeinmedizinisch und des sozialen Umfeldes), gefolgt von der kompletten intra- und extrabukkalen Untersuchung. Daraus ergibt sich eine Verdachtsdiagnose, die
von Fall zu Fall durch zusätzliche Massnahmen (Labor,
Biopsie und Histologie, verschiedene mikrobielle Kulturen) ergänzt werden muss. Dieses sequentielle Vorgehen
erlaubt es dem Zahnarzt (oder einem zugezogenen Spezialisten) eine definitive Diagnose zu stellen, und somit
eine adäquate Behandlung einzuleiten.
Zu den häufigsten Schleimhautveränderungen, wie sie im
Zusammenhang mit HIV-Infektionen beobachtet werden,
gehören in erster Linie die weissen Läsionen oder «white
lesions». Dabei muss zuerst differentialdiagnostisch zwischen Mundsoor (meist verursacht durch Pilze wie Candida) oder einer haarigen Leukoplakie unterschieden werden. Gewisse chronische Candida-Infektionen können dabei in Form von hyperkeratinisierten Läsionen auftreten.
Bei der Abklärung spielt die Anamnese eine wichtige
Rolle, weil Soorinfektionen meist durch Schmerzen,
Mundbrennen oder Juckreiz auffallen, während die «hairy
leukoplakia», hervorgerufen durch das Epstein-Barr-Virus (EBV), im Prinzip symptomlos verläuft. Im Fall einer
Candida-Infektion beruht die Diagnose auf einem direkten mikroskopischen Nachweis, wobei in gewissen Fällen
eine Kultur auf einem spezifischen Medium ergänzende
Aufschlüsse erbringt. Die durch das EBV verursachte Hyperkeratose ist durch eine entsprechende Biopsie und histologische Untrersuchung abzuklären.
Bei beiden Formen weisser Schleimhautveränderungen
treten auch Mischformen mit rötlichen Anteilen auf, wie
sie auch im Falle erythro-leukoplastischer Präkanzerosen
oder von Lichen planus beobachtet werden. Diese speziellen Krankheitsbilder müssen somit durch spezifische histologische Begutachtung ausgeschlossen werden (siehe
Tab. I).
Sowohl das Auftreten eines Soorbefalls wie auch einer
haarigen Leukoplakie treten meist im Zusammenhang mit
einer Immunschwäche auf, besonders bei HIV-Infektionen. Während die durch EBV bedingten Läsionen a priori
keiner speziellen Therapie bedürfen, sollten Candida-Infektionen immer mit fungizid wirkenden Medikamenten
behandelt werden, wobei aber Rezidive recht häufig auftreten.
Ulzeröse Schleimhautveränderungen im Mundbereich
stellen die zweithäufigste Gruppe von Läsionen dar, die
bei HIV-infizierten Patienten anzutreffen sind. Es handelt
sich meist um schmerzhafte Erkrankungen, die oft der eigentliche Grund der ersuchten Konsultation in der Zahnarztpraxis sind. Auch im Falle von oralen Ulzera muss der
präzisen Diagnosenstellung höchste Bedeutung beigemessen werden. Dies um so mehr, als es sich in vielen FälSchweiz Monatsschr Zahnmed, Vol. 107: 10/1997
869
Praxis – Fortbildung
len um Manifestationen infektiöser, oft hoch ansteckender Krankheiten handelt und somit eine systemische Ausbreitung oder Ansteckung von Drittpersonen durch geeignete Behandlung oder andere Massnahmen verhindert
werden muss.
Bei HIV-infizierten Patienten ist die Ätiologie ulzeröser
Veränderungen der Mundschleimhäute meistens eine Infektion durch Herpesviren, wobei das Herpes-simplex-Virus (HSV) weitaus am häufigsten anzutreffen ist. Es ist
festzuhalten, dass der Schweregrad und der Verlauf solcher Erkrankungen – obwohl in gewissen Fällen vergleichbar mit demjenigen von immunokompetenten Personen – im allgemeinen durch das Stadium der Immundefizienz wesentlich beeinflusst wird. Als ebenfalls auftretende Ursachen müssen das Herpes-zoster-Virus
(HZV) und insbesondere das Cytomegalovirus (CMV)
aufgeführt werden. Letzteres kann, von der Mundhöhle
ausgehend, zu schweren schmerzhaften Ulzera im Oropharynx und Ösophagus führen; im Falle der systemischen Ausbreitung besteht gar akute Lebensgefahr für den
Patienten, der einer sofortigen medizinischen oder stationären Behandlung zugeführt werden muss. Die Differentialdiagnose der viralen ulzerativen Läsionen beruht
im allgemeinen auf einer entsprechenden Biopsie und hi-
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Schweiz Monatsschr Zahnmed, Vol. 107: 10/1997
stologischen Untersuchung. In gewissen Fällen sollte
auch eine virologische Kultur durchgeführt werden.
Während durch Herpes verursachte Läsionen meist auf
die keratinisierten Schleimhautareale beschränkt bleiben,
treten aphtös bedingte Ulzera eher an nicht keratinisierten
Stellen auf. Ausser der klinischen Beobachtung kommt
auch der genauen Anamnese bei der Diagnosenstellung
grosse Bedeutung zu. Es gilt vor allem, kürzlich aufgetretene Verletzungen, die Einnahme systemisch wirkender Medikamente oder eine allfällige Leukopenie abzuklären. Allerdings kann die Ätiologie nicht in allen Fällen
festgestellt werden.
Last but not least muss in allen Fällen eventuell auftretender Ulzera mit isolierter Lokalisation ein maligner Tumor als Verdachtsdiagnose vermutet werden, besonders
wenn solche Läsionen keine oder eine schlechte Heilungstendenz aufweisen. Das Plattenepithelkarzinom ist
dabei das am häufigsten auftretende Malignom, und im
Falle anamnestischer oder klinischer Anhaltspunkte muss
der Abklärung dieser Diagnose absolute Priorität zugemessen werden.
(Zusammenstellung der ulzerösen Schleimhautveränderungen siehe Tab. II)