Copyright C Munksgaard 2001

J Clin Periodontol 2001; 28: 137145

Printed in Denmark . All rights reserved

ISSN 0303-6979

Classifications of oral lesions in

HIV infection

Nazanin Narani1 and Joel B. Epstein2

1

University of British Columbia, Vancouver,

BC, Canada, 2Department of Dentistry,
Vancouver General Hospital, Vancouver, BC,
Canada and University of Washington,
Seattle, WA, USA

Narani N, Epstein JB: Classifications of oral lesions in HIV infection. J Clin Periodontol 2001; 28: 137145. C Munksgaard, 2001.
Abstract
Background: Manifestations of immunosuppression may take the form of opportunistic infection, and neoplasia. While this paper has focused on gingival and
periodontal manifestations, these tissues cannot be evaluated in isolation. The
presence of involvement of other oral tissues such as the cheek or tongue with
manifestations associated with HIV such as hairy leukoplakia, Kaposis sarcoma
at these sites, and candidiasis in addition to periodontal manifestations may
further increase the clincial suspicion of underlying immunosuppression and/or
progression of the immunosuppressive state.
Discussion: The periodontist plays an essential role in identifying the periodontal
status of an individual and has an important role to play in early recognition
of signs and symptoms of HIV disease or progression of the medical condition.
Conclusion: Only through such recognition can appropriate definitive diagnostic
testing be conducted, and appropriate therapeutic intervention for the oral condition and the systemic condition be considered.

Oral and perioral lesions are common

in patients infected with human immunodeficiency virus (HIV), are often
the presenting feature, and may predict
deterioration in general health and a
poor prognosis (Scully et al. 1991).
Most HIV-infected patients have head
and neck manifestations at some stage
of disease (Rosenberg et al. 1989) and
oral lesions are often early signs (Schiodt & Pendborg 1989, Winkler & Robertson 1992). Most of these lesions are
considered opportunistic infections,
such as oral candidiasis and ulcers
caused by herpes simple virus. A broad
range of periodontal diseases has been
reported in HIV-infected persons including both common and less conventional forms of gingivitis and periodontitis, bacterial, mycotic and viral
infections, as well as neoplasms involving periodontium. Periodontists may
have patients with HIV/AIDS referred
to their offices for care. Due to multiple
oral conditions and periodontal involvement, periodontists are in a unique
position to recognize possible HIV in-

fection in its early stage and to be involved in the oral care of these patients.
Understanding of the epidemiology,
microbiology and natural history of
periodontal conditions associated with
HIV infection is limited partly due to
absence of reliable diagnostic criteria.
Several attempts have been made to develop rigid criteria including the one
proposed by Robinson et al. (1994)
with the purpose of distinguishing up
to 8 periodontal changes which may be
found in people infected with HIV.
A distinctive form of periodontitis
unique to HIV-infected individuals has
been described as a new entity characterized by a rapid onset, progression
and destruction of both soft and hard
tissue, in contrast to the common
slowly progressing form of adult periodontitis (SanGiacomo et al. 1990).
Rapidly progressive periodontitis has
been implicated to be one of the first
clinical presentations of previously undiagnosed HIV infection. Although the
situation does not predictably respond
to conventional treatments of scaling

Key words: periodontal involvement; oral

lesions; HIV
Accepted for publication 28 February 2000

and root planning and improved oral

hygiene, with proper diagnosis and
prompt aggressive management using
adjunctive agents, considerable success
may be achieved.
Changes in medical therapy have led
to improved prognosis for those infected by HIV, although it appears that
over time resistance to the current approaches to therapy develops and progression of immunosuppression will occur. The current therapy has improved
both the quantity and the quality of life
for infected individuals, however does
not represent a cure. Because of this, increasing numbers of individuals will be
in the community requiring oral, dental
and periodontal management. The recent introduction of protease inhibitors
and anti-viral drugs, have changed frequency and severity of oral manifestations of HIV over time. It is expected
that there will be a recurrence of oral
signs and symptoms associated with resistance of HIV to current therapeutic
protocols. Improvements in host immune response due to new medications

138

Narani & Epstein

have reduced the frequency of oral conditions such as candidiasis and Kaposis
sarcoma, however, virus resistance to
anti-viral drugs over time may increase
the incidence of malignant diseases and
opportunistic infections with advancing
disease (Epstein et al. 1998). There are
increasing numbers of patients living
with immunosuppression. The numbers
of HIV positive patients who may seek
care are increasing. Thorough oral examinations are essential for early recognition of disease progression and comprehensive evaluation of HIV-infected
patients.
The first classification of the oral
manifestations associated with HIV-infection was based on etiological aspects
and distinguished between lesions
caused by fungi, bacteria, viruses, neoplastic lesions, and other alterations
(Pindborg 1989). In 1990, the classification was modified to establish three
main groups: (1) lesions strongly associated with HIV-infection, (2) lesions less
commonly associated with HIV-infection, and (3) lesions seen in HIV-infection (EEC-Clearhouse on oral problems
related to HIV-infection and WHO collaborating center on oral manifestations of the human immunodeficiency
virus. 1991). Modified versions of this
classification have since been proposed
(EEC-Clearhouse and WHO on oral
manifestations of HIV, 1993).
The goal of this review is to present
the more common oral manifestations
of HIV infection with emphasize on the
disorders affecting the periodontal
tissues of HIV-seropositive individuals.
Oral Candidiasis

Oral candidiasis is a common early

manifestation of HIV infection. Candida albicans is the predominant species, but C. tropicalis, C. glabrata, and
C. krusei occur occasionally and this diversity has implications for choice of
and response to therapy (Greenspan &
Greenspan 1996).
Erythematous candidiasis

The erythematous form of candidiasis

presents as red areas with high rate of
occurrence on the palate and dorsum of
the tongue which are occasionally
mixed with white spots. Detection of
Candida albicans and/or response to
anti-fungal therapy may be useful in an
absolute diagnosis, although definitive
criteria do not exist for this condition.

Pseudomembranous candidiasis

The condition is characterized by presence of white or yellow spots or plaques

with similar rate of occurrence in different parts of oral cavity. The surface can
be removed leaving a red bleeding surface. Definitive criteria include response
to anti-fungal therapy and presence of
Candida albicans detected by smears or
culture, which the latter is not essential
for diagnosis (Fig. 1).
Angular cheilitis

This is another form of oral candidiasis, occurs as cracking, fissuring, and

redness at the commissures; these
lesions may be unilateral or bilateral
and may be seen in association with any
of the intraoral presentations.
Although Candida albicans infections
arise frequently on the check, the palate, the dorsum of the tongue, and the
corner of the mouth, gingivo-periodontal manifestation is more unusual.
Periodontal Disease

The first report indicating an association between HIV-infection and periodontal diseases was published in 1985
(Dennison et al. 1995). Since then numerous reports have been added to the
literature and several attempts have
been made to classify the diversity of
manifestations. The periodontal diseases in HIV-seropositive patients include common as well as less conventional forms of gingivitis and periodontitis. Winkler et al. in (1992)
published a review paper reporting the
distinguishing features, microbiology
and treatment of severe periodontal diseases that are observed in HIV-infected
persons including HIV-associated gingivitis, HIV-associated periodontitis and
necrotizing stomatitis of periodontal
origin. The updated classification of
EC-Clearhouse on HIV-related periodontal disease includes 3 conditions:
(1) linear gingival erythema, (2) necrotizing ulcerative gingivitis (NUG) and
(3) necrotizing ulcerative periodontitis
(NUP). All 3 conditions are clinical diagnosis without definitive criteria.
Holmstrup et al. (1994) proposed a
descriptive classification to overcome the
previously inconsistent classification
and terminology given to HIV-associated periodontal conditions and characterized them according to established
periodontal disease entities that will be

reviewed in this paper. The reported

prevalence of periodontal disease in
HIV-infected patients varies greatly in
the literature, as it depends on many factors such as stage of the disease and the
risk group to which the patient belongs.
In a study of the oral manifestations in
396 Spanish patients with HIV-infection,
the most common oral disorders were related to periodontal disease with the
prevalence of 78.3% (Ceballos-Salobrena et al. 1996). On the other hand, oral
manifestations of the immunodeficiency
virus, were studied in 600 consecutive
HIV-infected patients in South Africa,
and combined gingival/periodontal
lesions were reported in only 8.5% of the
patients (Arendorf et al. 1998). According to Holmstrup et al. (1994), the common manifestations of disorders affecting the periodontal tissues of HIV-seropositive individuals include:
Gingivitis

Gingivitis associated with bacteria and

yeast
Conventional chronic gingivitis. This
condition is characterized by red to bluish red, edematous gingival tissue
usually with swollen interdental papillae and increased tendency to bleeding.
Swango et al. (1991), showed significantly more bleeding sites and destruction of interdental papillae in HIV-seropositive patients with more than 400
CD4 T-cell counts compared to those
with counts of less than 400. Therefore,
the relation between gingivitis, microflora and immune status is not clear.
Chronic gingivitis with band shaped/
or punctate erythema. This condition is
described as distinctive erythema of the
free gingiva, attached gingiva and alveolar mucosa. Two of the most prominent features of this condition are linear
erythematous band involving the free
gingival margins and punctate or diffuse erythema of the attached gingiva.
The free gingiva tends to hemorrhage
spontaneously, while the associated
teeth usually have only light plaque formation. The strong resistance of this
gingivitis to the usual local treatment
measures is striking. The differential diagnosis includes conventional chronic
gingivitis, oral lichen planus (Holmstrup et al. 1989), mucous membrane
pemphigoid (Pindborg 1992), and gingivitis like changes due to thrombocytopenia (Pindborg 1989). Studies conducted by Barr et al. (1992) and Swango
et al. (1991) revealed no correlation be-

Classifications of oral lesions in HIV infection

139

Fig. 1. Irregular leukoerythroplakia of residual alveolar ridge mucosa

that will not wipe off the surface along the ridge, although on the
floor of the mouth mucosa white patches that are removable are seen.
Culture and biopsy revealed pseudomembranous candidiasis and
hyperplastic candidiasis involving gingival tissues.

Fig. 4. Patient presents with sensitivity, spontaneous bleeding and

multiple 1 mm rounded ulcerations involving gingival tissues consistent with herpetic gingivostomatitis.

Fig. 2. This case presents findings of band-shaped gingival erythema

involving the lower gingival tissues as well as diffuse periodontal bone
loss which was advanced between the upper incisors.

Fig. 5. Intraoral clusters of 1 mm rounded ulcerations of herpes simplex virus.

Fig. 3. Necrotizing ulcerative gingivitis involving all gingival surfaces,

fascial, interproximal and lingual.

Fig. 6. Extensive ulceration of gingival margins in an immunosuppressed patient with progressive herpes simplex virus infection.

tween immunosuppression and this

condition since equal numbers of cases
had CD4 T-cell counts above and be-

low 400/mm (Schiodt & Pindborg

1987). The microbiological findings of
HIV-associated gingivitis are consistent

with that of conventional periodontitis

and different from that of conventional
gingivitis that suggests a close relation-

140

Narani & Epstein

ship between this gingivitis form and

periodontal breakdown (Murray et al.
1991) (Fig. 2).
Necrotizing Gingivitis (NG). In HIVinfected patients, the condition has
been described as red and swollen gin-

giva with yellowish-grayish marginal

areas of necrosis with loss of interdental
papillae (Schiodt & Pindborg 1987)
which usually takes a chronic or subacute course. Characteristic of HIVNUG is its rapid progression and con-

version to necrotizing periodontitis.

Left untreated, or in the course of an
increasingly altered immune resistance,
such gingivitis can resolve into progressive periodontitis, which is characterized by its extremely rapid pro-

Fig. 7. This case presents an exophytic pedunculated mass diagnosed

as a condyloma involving the gingival margin.

Fig. 10. Panoramic radiograph demonstrating irregular pattern of

bone loss in HIV-P.

Fig. 8. Manifestations of rapid attachment loss in 24-year-old male.

Fig. 11. Ulceration with exposure of bone and intense erythema is

seen in the interdental region of the lower molars.

Fig. 9. Attachment loss with interdental necrosis, and increased probing depths.

Fig. 12. Isolated involvement of the upper gingiva between incisors

and between canine and first bicuspid with minimally visible lesions
of KS.

Classifications of oral lesions in HIV infection

gression and destruction of the periodontal and bony substances, usually
accompanied by severe pain. The relationship between immune status and
development of NG is not clear. The
disease was unrelated to immunosuppression with equal number of patients
having CD4 T cell counts above and
below 400/mm3 (Barr et al. 1992). On
the other hand, in a study of 390 US
HIV-seropositive soldiers, the presence
of NG was correlated with a depleted Tlymphocyte count (400/mm3) but not
with the Walter Reed staging level
(Thompson et al. 1992). Recently, Patton & McKaig (1998) reported a case
of rapidly progressive periodontal tissue
breakdown and bone loss in an HIV-infected markedly immunosuppressed
homosexual male. Within 6 months of
initial presentation with a necrotizing
ulcerative gingivitis, the lesion extended
to a necrotizing ulcerative stomatitis involving the surrounding periodontium

and palatal mucosa; the alveolar bone

loss resulted in tooth mobility necessitating extraction of 2 involved teeth.
Little is known about the microbiology
of HIV-associated NG, however, Borrelia, grampositive cocci, (-hemolytic
streptococci, C. albicans as well as cytomegalovirus have been isolated from
the lesions (Reichart et al. 1987; Sabiston 1986) (Fig. 3).
Gingivitis caused by virus
Herpetic gingivostomatitis. Viral shedding into the oral environment is common in immunosuppressed patient. The
majority of oral and perioral herpes
simplex infections are caused by HSV1, but may also be due to HSV-2 associated lesions in HIV-infected individuals
(Schiodt & Pindborg 1987). The primary type of lesions are more common
in HIV-infected patients compared to
recurrent intraoral herpes infections.
The condition is characterized by gingi-

141

val, palatal, dorsal tongue and occasionally mucosal vesicles which rupture and leave painful irregular 12 ulcers often in clusters. The definitive
diagnosis is made by viral isolation in
tissue. Viral culture could be positive
but will not confirm the cause of tissue
change due to frequent asymptomatic
shedding (Figs. 46).
Herpes zoster. The condition is
caused by varicella zoster virus and it
may indicate a poor prognosis of HIV
infection (Scully et al. 1991). The
characteristic clinical manifestation of
disease is unilateral occurrence of the
vesicles or ulcers in mucosa and/or skin
corresponding to the area of innervation by a branch of trigeminal nerve
(Greenspan et al. 1990). The lesions are
extremely painful and the course of the
disease may extend to the bone leading
to osteonecrosis (Schwartz et al. 1989).
Other viral infections. Progressively
destructive oral ulcerations appearing

Fig. 13. Discolored and enlarging lesion involving palatal gingiva and
palatal mucosa in the upper molar region.

Fig. 15. A pink, firm mass is seen arising from the gingiva diagnosed
as non-Hodgkins lymphoma.

Fig. 14. Gingival involvement diagnosed as Kaposis sarcoma resulting in gingival enlargement covering the crowns of teeth with tissue
ulceration.

Fig. 16. Gingival infiltration in patient with non-Hodgkins

lymphoma.

142

Narani & Epstein

like punched-out lesions can indicate

disseminated infections with cytomegalovirus. The diagnosis can be established histologically on the basis of the
typical shape of cytomegalovirus-infected cells and the immunohistochemical demonstration of the virus antigen
(Langford et al. 1990).
Furthermore, changes due to human
papillomavirus may occur as verruca
vulgaris, condylomata accuminatum, or
focal epithelial hyperplasia (Langford
et al. 1994) (Fig. 7).
Periodontitis

HIV-associated periodontitis comprises

a wide range of conditions. The manifestations include: conventional adult
periodontitis (Friedman et al. 1992),
rapidly progressive periodontitis (Reichart et al. 1987), periodontitis with
soft tissue loss and irregular bone destruction in an otherwise clean mouth
(EEC-Clearhouse 1993) and gingival
features of HIV-associated gingivitis associated with necrosis of gingival/periodontal attachment apparatus and rare
spontaneous resolution (Winkler and
Robertson 1992).
Periodontitis associated with bacteria
and yeast
Conventional adult periodontitis/rapidly
progressive periodontitis. The condition
is associated with rapid destruction of
the periodontal attachment in addition
to the features of HIV-associated gingivitis. Most studies have found an association of progressive periodontitis
and decreased number of peripheral Thelper cells. In a study conducted by
Lucht et al. (1991) periodontitis in patients with more advanced stages of
HIV-infection was related to severity of
systemic disease and to decreasing numbers of CD4 lymphocytes but not to
a visible plaque index or occurrence of
periodontal pathogenic micro-organisms. In a prospective study of 20
months duration in 114 male HIV-positive cohorts, CD4 counts200/mm3
conferred a 6-fold increased risk of
attachment loss of 3 mm or more compared with CD4 counts 200/mm3
(Barr et al. 1992). In contrast, alveolar
bone levels were studied from intraoral
radiographs in AIDS and HIV-seropositive patients and in control subjects
and it was reported that the extent of
alveolar bone loss, number and extent
of vertical defects and furcation invasions were not associated with HIV

status (Persson et al. 1998). Several reviews published on the oral findings in
HIV-infected subjects (Lamster et al.
1995, Winkler 1995) suggest that periodontitis in HIV-infected individuals is
likely to have a more common clinical
and radiographic appearance than that
associated with necrotizing periodontitis (will be discussed next) despite
the fact that some uncommon microorganisms may be isolated from periodontal microflora of HIV-infected patients (Zambon et al. 1995). Several
studies have indicated that HIV-associated gingivitis and periodontitis sites
harbor periodontal pathogens significantly more frequently than sites in
HIV-negative subjects. However, microbiota found in HIV-associated periodontitis does not differ qualitatively
from conventional adult periodontitis
(Murray et al. 1988, Murray et al.
1989). Patients born with T-cell defects
such as DiGeorge syndrome characteristically suffer from cutaneous mycotic
infections. Thus, as an HIV patient begins to lose T-cell function, opportunistic species including C. albicans may
gain advantage. This is also demonstrated in immunosuppressed patients
on large dosage of steroids which deplete lymphocytic cell populations (Salvi et al. 1998) (Figs. 810).
Necrotizing periodontitis (NP)
The clinical manifestations at the initial
stage are changes in gingival contour
such as interproximal necrosis, ulceration and cratering. Foetor is present in
most cases. Severe, deep pain, localized
in the jaw bone is considered as an important feature of HIV-associated NP
and the chief reason for the patient to
seek treatment. Spontaneous bleeding
of the involved sites is another prominent feature of the disease. One of the
most distinguishing features is soft
tissue necrosis and rapid destruction of
periodontal attachment and bone
(Winkler et al. 1988). Usually the disease affects several localized areas independently, however severe cases can affect all of the teeth. Due to the extensive
gingival necrosis that often coincides
with loss of crestal alveolar bone, deep
pocket formation associated with the
lesions is not usual. The rapid progression of the tissue necrosis sometimes leads to exposure of alveolar bone
which becomes sequestrated and leaves
deep interdental craters (Holmstrup &
Westgaard 1994). Prevalence rates of
NP in HIV-infected cohorts vary from

0% to 18% due to the diversity of the

evaluated populations, methods, and
diagnostic criteria used (Masouredis et
al. 1992, Riley et al. 1992). Current estimates of prevalence of NP in HIV seropositive populations are 5% or less
(Lamster et al. 1997). Immunological
studies have shown significant reduction
of T-cells in gingival tissue of HIV-infected patients with periodontitis.
Steidley et al. (1992) found a complete
absence of T-cells in gingival tissue of
HIV-infected patients with NP. Glick et
al. (1994) reported that patients with
NP were 20.8 more likely to have a
CD4 cell count200/mm3 than were
patients who did not present with NP
suggesting that the impairment of local
immune defense could explain the
rapidly progressive nature of periodontitis in these patients. In addition
to the depletion of peripheral blood Thelper lymphocytes, the alterations in
the local host response to the subgingival microflora appears to be related to
an increase in inflammatory mediators
such as IL-1b (Lamster et al. 1998) as
well as, an accumulation of hypersensitive polymorphonuclear leukocytes
(Ryder et al. 1988). In some instance,
especially in patients who do not receive
treatment or who have reduced defense
mechanisms, inflammation of the surrounding soft tissue may occur, leading
to the clinical appearance of a nomalike change. Such necrotic regions of
tissue, form favorable conditions for
the multiplication of unusual opportunistic agents, such as mucormycoses that
is a progressive mycotic infection. The
organisms enter the vessels, cause
thromboses, and lead to rapidly progressing destruction of the surrounding
hard and soft tissues in a matter of
weeks. The course of the disease is fulminant and is associated with a high
mortality (Langford et al., 1994). Although several studies have found similar microflora from both NP and classical adult periodontitis, there is evidence
of involvement of microorganisms
atypical for the subgingival microflora
of adult periodontitis in NP. Ram et al.
(1991),
have
isolated
yeasts,
pseudomonads, enteric rods and other
non-oral bacteria from NP lesions. In a
recent review by Lamster et al. (1997)
the authors suggested that progression
of periodontal disease in HIV-infected
individuals was dependent upon the immunologic competence of the host and
the local inflammatory response to both
typical and atypical subgingival micro-

Classifications of oral lesions in HIV infection

flora. Further studies are required to
elucidate the etiologic and pathogenetic
aspects (Fig. 11).
Hairy leukoplakia (HL)

The lesion of HL is seen in about one

fourth of HIV-infected persons (Silverman et al. 1986) and is characterized
by presence of white to gray lesions
located bilaterally on the lateral margins of the tongue which can not be removed and may extend to the ventral
and dorsal surfaces of the tongue and
less commonly involve buccal mucosae.
Definitive criteria include presence of
Epstein-Barr virus or lack of response
to anti-fungal treatment (Scully et al.
1991).
Neoplasms

Kaposis sarcoma (KS) is the most common malignancy associated with HIV
infection and is oral and perioral in
50% or more of patients with mucocutaneous KS (Rosenberg et al. 1984).
Oral KS typically presents as red-bluish
swellings with or without ulceration
which are most common on the palate,
gingiva and dorsal tongue. Gingival involvement occurs in 23% of cases
(Greenspan & Greenspan 1987). In a
study of 33 patients with KS, gingival
KS was seen predominantly on the labial or buccal gingiva and on the attached gingiva and gingival margin
(Epstein & Scully 1991). The tumor initially manifests as a red purple or bluish
patch which later presents as nodules
resembling hemangioma or a peripheral
giant cell granuloma. The lesions arise
initially in the subepithelial or submucosal connective tissue and pathologic
changes of the bone or the periodontal
tissue can be seen only after some
growth of the tumor. Diffuse osteolysis
in the region of the alveolar bone and
expansion of periodontal spaces are
found only during late, exophytically
growing KS (Langford et al. 1989). The
progression of the lesion to nodular
form is associated with increasing
grades of immunosuppression (Petit et
al. 1986).The differential diagnosis include amalgam tattoo, hemangioma,
lymphangioma, giant-cell granuloma,
oral nevi, and hyperpigmentation. Diagnosis is made by histological appearance on biopsy (Figs. 1214).
Non-Hodgkins lymphoma (NHL) is
the second most common malignancy
in HIV-infection and is characterized by

firm elastic swelling that usually is red

or purple in color and can be ulcerated.
The most common sites are gingiva,
palate and fauces. Cases have been presented in which a gingival lesion was
the first manifestation of AIDS (Rubin
et al. 1989). Initially, the lesion may
present as a pink gingival mass, may resemble acute gingival inflammation and
further progression of disease may include a whitish verrucous surface or necrosis of gingiva resembling ANUG
(Holmstrup & Westgaard 1994). Oral
NHL may be misinterpreted as KS, and
the differential diagnosis is important
because it significantly affects the
choice of treatment (Brahim et al.
1989). Definitive criteria include histological features on biopsy as well as immunocytochemical tests (Greenspan et
al. 1992) (Fig. 15, 16).
Xerostomia

Some HIV-infected persons in an early

stage of infection experience xerostomia
(Schiodt et al. 1992). Xerostomia may
be associated with HIV disease and
may be a complication of prescribed
medication that may be xerostomic. A
sicca-type syndrome termed as HIVsalivary gland disease has been described in HIV patients and associated
with diffuse infiltrative CD8 lymphocytosis (Lebovits et al. 1989). The disease is characterized by diffuse enlargement of the major salivary glands and/
or xerostomia. CMV has been demonstrated in the salivary gland of xerostomic patients (Greenspan et al. 1992).
There is no evidence of HIV and EBV
in the glands. Identification of the dry
mouth and reduced saliva production
can also lead to further investigation
and diagnosis and requires management in order to control the conditions
associated with a dry mouth including
increased risk of candidiasis and caries
risk. In addition, management of xerostomia will improve oral comfort, may
affect the quality of speech, and affect
the use of any prosthesis.
Pain

HIV-Infection can involve every organ

system and cause organ-specific symptoms as well as non-specific systemic
symptoms. Pain may cause considerable
disability, discomfort and impaired
quality of life. Pain associated with HIV
disease has been estimated to be equal
to the frequency and severity of cancer

143

related pain. According to ONeil &

Sherrard (1993), Schofferman (1989),
approximately 50% of patients infected
with HIV admitted to hospital suffer
from pain-related syndromes. The most
frequently reported pain syndromes are
chest pain, headache, abdominal pain,
oesophageal and oral cavity pain, pain
related to peripheral neuropathies and
musculoskeletal pain. Oral cavity pain
is experienced by 28% of HIV-infected
individuals (Schofferman 1989) and
may be due directly to mucosal disease,
a side effect of medications that have
neurotoxic effects including some antivirals, and neuropathy that can be related to the anti-viral therapies or other
medications and direct effect of HIV or
neurologic function. The dentist must
be aware that peripheral neuropathy
may present as jaw pain or toothache,
and therefore specific findings of dental
pathosis should be present prior to considering dental interventions in these
patients. The most common cause of
oral cavity pain is oral candidiasis. Bacterial infections are mainly seen as necrotizing gingivitis, resulting in rapid destruction of periodontium and alveolar
bone that can lead to pain, tooth mobility and loss. Dental abscesses occur
more commonly in HIV-infected individuals than in the general population.
Herpes simplex virus stomatitis, herpes
zoster radiculitis, recurrent aphthous
lesions and Kaposis sarcoma also cause
oral pain (Pensfold & Clark 1992). The
optimal management of HIV-related
pain consists of treating any correctable
cause of pain with surgery, antiviral,
antifungal or antibiotic agents in conjunction with a NSAID or acetaminophen to control mild to moderate pain.
If the pain is not adequately controlled,
an opioid may be prescribed.
Neurologic disorders associated
with HIV-infection

Neurologic disease occurs frequently in

patients infected with HIV. This can be
either directly related to CNS infection
by HIV and include HIV-associated dementia and other CNS diseases such as
myopathy and the neuropathies or related to the immunosuppression associated with the disease that may result in
opportunistic infections and neoplasms
of the central nervous system, as well as
metabolic derangement and medications (Atkinson & Grant 1994). HIVassociated dementia is a common neurologic complication and is character-

144

Narani & Epstein

ized by cognitive, motor and behavioral

changes (Kieburtz & Schiffer 1989).
Difficulty with memory has implications with respect to careful and thorough presentation of instructions for
care, and frequent reminders of appointments that may be scheduled. At
present, no specific therapy is available
for this disorder.
Zusammenfassung
Klassifikation der oralen Lasionen bei HIVInfektion
Manifestationen einer Immunsuppression
konnen die Form einer opportunistischen Infektion und Neoplasie annehmen. Wahrend
diese Publikation auf gingivale und parodontale Manifestationen fokusiert war, konnen
diese Gewebe nicht isoliert betrachtet werden. Die Prasenz der Einbeziehung von anderen oralen Geweben, wie z.B. die Wangen
oder die Zunge mit Manifestationen, die mit
HIV assoziiert sind, wie Haarleukoplakie,
Kaposis Sarkom an diesen Stellen und Candidiasis zusatzlich zu parodontalen Manifestationen, konnen weiterhin den klinischen
Verdacht einer zu Grunde liegenden Immunsuppression und/oder progression des immunsuppressiven Status verstarken. Der Parodontologe spielt eine groe Rolle in der
Diagnostik des parodontalen Status eines Individuums und hat eine wichtige Rolle in der
fruhzeitigen Entdeckung von Zeichen und
Symptomen der HIV-Erkrankung oder Progression der medizinischen Verhaltnisse. Allein durch diese Anerkennung kann das definitive diagnostische Testsystem ausgewahlt
werden und die passende therapeutische Intervention fur die oralen und systemischen
Bedingungen bestimmt werden.

Resume
Classifications des lesions buccales dans linfection au VIH
Les manifestations de limmunosuppression
peuvent prendre la forme dinfections opportunistes et de neoplasies. Bien que cet article
sinteresse aux manifestations gingivales et
parodontales, ces tissus ne peuvent etre evalues isolemment. La presence de limplication
dautres tissus oraux comme la joue ou la
langue avec des manifestations associees aux
VIH comme la leucoplasie chevelue, des sarcomes de Kaposi sur ces sites, et des candidoses en plus des manifestations parodontales
peut augmenter davantage la suspicion clinique dimmunosuppression sous jacente et/ou
la progression dun etat immunosuppressif.
Le parodontiste joue un role essentiel dans
lidentification de letat parodontal dun individu et a un role important a` jouer dans la
reconnaissance precoce des signes et des
symptomes de la maladie du VIH ou la progression des conditions medicales; il ny a
que par cette reconnaissance quun test diagnostic definitif appropie peut etre realise et

quune intervention therapeutique vis-a`-vis

des conditions orales et systemiques puisse
etre consideree.

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Address:
J. Epstein
Department of Dentistry
Vancouver General Hospital
855 West 12th Avenue
Vancouver, BC V5Z 1M9
Canada
Fax 1 604 875 4791