AIDS and Periodontium

AIDS and the Periodontium
AIDS
Acquired immunodeficiency syndrome.

First reported in 1981.
Human immunodeficiency virus.
Profound impairment of the immune system
(CD4 cell).
Increased risk for malignancy, disseminated
infections and adverse drug reactions.
high quantities of HIV only in blood, semen, and
cerebrospinal fluid.
Modes of Transmission
Risk Groups-Healthcare Professionals
CDC AIDS Surveillance Case Definition

(1993)
All HIV-infected persons who have
> 200 CD4+ T-lymphocytes/uL, or
> 14% CD4+ T-lymphocyte.
Criteria for HIV infection for persons ages > 13 years:
repeatedly reactive screening tests for HIV antibody
(e.g., enzyme immunoassay) with specific antibody
identified by the use of supplemental tests (e.g.,
Western blot, immunofluorescence assay);
direct identification of virus in host tissues by virus
isolation; c) HIV antigen detection; or d) a positive
result on any other highly specific licensed test for
HIV.
CDC Surveillance Case

Classification
1. CD4+ T-Lymphocyte Categories
Category 1: greater than or equal to 500 cells/mL
Category 2: 200-499 cells/uL
Category 3: less than 200 cells/uL
2. Clinical Categories
Category A
Asymptomatic HIV infection
Persistent generalized lymphadenopathy
Acute (primary) HIV infection with accompanying
illness or history of acute HIV infection
Category B
Bacillary angiomatosis
Candidiasis, oropharyngeal (thrush)
Candidiasis, vulvovaginal; persistent, frequent, or
poorly responsive to therapy
Cervical dysplasia (moderate or severe)/cervical
carcinoma in situ
Constitutional symptoms, such as fever (38.5 C)
or diarrhea lasting greater than 1 month
Hairy leukoplakia, oral

Herpes zoster (shingles), involving at least two
distinct episodes or more than one dermatome
Idiopathic thrombocytopenic purpura
Listeriosis
Pelvic inflammatory disease, particularly if
complicated by tubo-ovarian abscess
Peripheral neuropathy
Category C
Clinical conditions listed in the AIDS surveillance
case definition.
Symptoms
Few weeks to months.
Acute symptoms-malaise, fatigue, fever, myalgia,
erythematous cutaneous eruption, oral
candidiasis, oral ulcerations, and
thrombocytopenia.
Duration - 2 weeks.
Seroconversion occurs 3 to 8 weeks later.
Oral Manifestations
Commonly occuring oral candidiasis
oral hairy leukoplakia
atypical periodontal diseases
oral Kaposi's sarcoma, and
oral non-Hodgkin's lymphoma
Less common - melanotic hyperpigmentation,
mycobacterial
infections, necrotizing ulcerative stomatitis, miscellaneous
oral ulcerations, and viral infections.
Oral Candidiasis
Most common - 90% of AIDS patients.
Diminished host resistance
debilitated patients , patients
receiving immunosuppressive therapy.
Oppurtunistic prolonged antibiotic
therapy.
Most oral candidal infections (85% to
95%) are associated with Candida
albicans.
Non-C. albicans infections are more
common among immunocompromised
individuals already receiving
antifungal therapy for C. albicans.
Pseudomembranous candidiasis (thrush)

painless or slightly sensitive white lesions
readily scraped and separated from the surface of the oral mucosa
Hard and soft palate and the buccal or labial mucosa
Erythematous candidiasis
red patches on the buccal or palatal mucosa
associated with depapillation of the tongue
Hyperplastic candidiasis
least common
buccal mucosa and tongue
resistant to removal
Angular cheilitis
commissures appear erythematous
surface crusting and fissuring
Diagnosis
microscopic examination of a tissue sample or smear.
hyphae and yeast forms.
Treatment
topical and systemic antifungal agents.
Amphotericin B oral suspension is more effective
against
Candida albicans.
Ketaconazole-systemic therapy.
refractory or recurrent.
30% of AIDS related candidiasis relapse within 4 weeks
of treatment and 60% to 80% within 3 months .
Oral Hairy Leukoplakia

primarily occurs in persons with HIV
infection
lateral borders of the tongue,
bilateral distribution
asymptomatic, poorly demarcated
keratotic area
Size - few millimeters to several
centimeters
corrugated appearance characteristic vertical striations
Microscopically, the lesion shows a
hyperparakeratotic surface,
acanthosis, koilocytes (containing
Epstein-Barr virus)
surface colonization by Candida
organisms
EBV-infected but HIV-negative individuals suffering

from immunosuppressed conditions (e.g., acute
myelogenous leukemia, organ transplantation or
extensive systemic corticosteroid therapy).
OHL of the tongue in a high-risk patient is
considered to be a specific early sign of HIV
infection and a strong indicator that the patient
will develop AIDS.
83% of HIV-infected patients with hairy leukoplakia
would develop AIDS within 31 months, and
Nearly 100% of patients with hairy leukoplakia will
eventually develop AIDS.
Treatment
Laser or conventional surgery.
systemic antiviral agents such as acyclovir.
Kaposis Sarcoma
Multifocal, vascular neoplasm.
Probable causative organismhuman herpes virus-8 (HHV-8).
HIV-infected individuals are
7000-fold more likely to
develop KS.
localized and slowly growing
lesion. In HIV individuals aggressive lesion.
Majority (71%) develop lesions
of the oral mucosa, particularly
the palate and gingiva.
Painless, reddishpurple macules of the

mucosa.
Nodules, papules, or nonelevated
macules that are usually brown, blue,
or purple.
Microscopic features
Atypical vascular channels
extravascular hemorrhage with
hemosiderin deposition
spindle cell proliferation in association
mononuclear inflammatory infiltrate
consisting mainly of plasma cells
Presence of KS signifies transition to outright AIDS.
Differential Diagnosis
Pyogenic granuloma, hemangioma, atypical
hyperpigmentation, sarcoidosis, bacillary angiomatosis,
angiosarcoma, pigmented nevi, and cat-scratch disease.
Management
Antiretroviral agents, laser excision, radiation therapy, or
intralesional injection with vinblastine or interferon a.
Tendency to recur.
Destructive periodontitis scaling and root planing.
Atypical Periodontal Diseases

More common in HIV-infected
i.v. drug users.
Related with poor oral
hygiene and lack of dental
care.
Linear Gingival Erythema
persistent, linear, easily
bleeding, erythematous
gingivitis.
localized or generalized;
marginal or diffuse.
Concomitant oral candidiasisCandida dubliniensis.
Histopathology
Increased blood vessels.
Lack of infammatory cell infiltrate.
Treatment
Non-responsive to therapy.
Spontaneous remission-some cases.
Meticulous oral hygiene.
Scaling, irrigation with chlorhexidine.
Recall after 2-3 weeks.
Persistent cases-treat for candida infection.
Necrotising Ulcerative Gingivitis

Inflammatory destructive gingival
condition.
Ulcerated, necrotic papillae-punched-out
appearance.
yellowish-grayish white sloughpsuedomembrane.
Lesions develop rapidly, painful.
Bleeding-spontaneous or on slight
provocation.
Foul breath-pronounced.
Histopathology - Fibrin deposits, leukocytes,
erythocytes, masses of bacteria.
Necrotising Ulcerative Periodontitis

Extension of NUG.
Rapid bone loss and
periodontal attachment
loss.
Usually localized to a few
teeth.
Bone is exposed with
sequestration.
May undergo spontaneous
remission.
Interproximal craters.
Necrotizing Ulcerative Stomatitis

Necrosis of significant areas
of oral soft tissue and
underlying bone.
Severely destructive and
acutely painful.
Severe depression of CD4
cells.
Similar to cancrum oris
(noma).
Management
Cleaning and debridement.
Oral hygiene instructions.
Systemic antibiotics-metronidazole and
amoxycillin.
Re-evaluation after 1 month.
Osseous necrosis - remove the affected bone to
promote wound healing.

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AIDS and Periodontium

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AIDS and the Periodontium

Acquired immunodeficiency syndrome.

Risk Groups-Healthcare Professionals

CDC AIDS Surveillance Case Definition

CDC Surveillance Case

Hairy leukoplakia, oral

Pseudomembranous candidiasis (thrush)

Oral Hairy Leukoplakia

EBV-infected but HIV-negative individuals suffering

Painless, reddishpurple macules of the

Presence of KS signifies transition to outright AIDS.

Atypical Periodontal Diseases

Necrotising Ulcerative Gingivitis

Necrotising Ulcerative Periodontitis

Necrotizing Ulcerative Stomatitis

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