HIV & AIDS part 2 Flashcards
- As a — pathogen it has important implications for dental practitioners.
bloodborne
The average dental practice is predicted to encounter at least — patients
infected with HIV per year.
two
In the United States, –% of individuals who have
acquired HIV are unaware of their status,
contributing to as high as –% of continuous HIV
spread.
15
40
The risk of HIV transmission from infected patients to
health care workers is very low, reportedly about – of
every 1000 cases (–%) through a – or other
sharp instrument contaminated with the virus
3, 0.3
needlestick
In comparison, the risk of infection from a needlestick is –% for hepatitis B and
is –% for hepatitis C
30
3
The CDC recommends — as soon as possible after
exposure to HIV-infected blood, regimen recommended is based on the severity
of the exposure and the HIV status of the source patient (two- vs three- drug
regimen of antiretroviral medication).
postexposure prophylaxis (PEP)
A less severe exposure (i.e., superficial), an
asymptomatic source patient or has a low viral load
(<1500 viral copies/mL) use a
two-drug PEP.
A more severe exposure (i.e., deep), or when the
patient is symptomatic, has AIDS, or a high viral load
use of at least a
three-drug PEP.
- Tests for seroconversion should be performed at
3, 6, and 12 months.
There have been six reports of occupational HIV
seroconversion despite combination postexposure
prophylaxis.
* Transmission from health care provider to patient has
occurred. The risk of transmission from healthcare
personnel to patients is also minimized by
adherence
to standard infection control procedures.
Standard precautions are a set of infection control practices used to prevent transmission of diseases that can be acquired by contact with (4)
blood, body
fluids, non-intact skin (including rashes), and mucous membranes.
- — must be used for all patients.
Standard precautions
o Dentists are key stakeholders in facilitating the elimination of the stigma associated with the
infection.
o Several guidelines have emerged regarding the rights of dentists and patients with AIDS,
including the following:
- Dental treatment may not be withheld if the patient refuses to undergo testing for HIV exposure.
- A patient with AIDS who needs emergency dental treatment may not be refused care simply
because the dentist does not want to treat patients with AIDS. - No medical or scientific reason exists to justify why patients with AIDS who seek routine dental
care may be declined treatment by the dentist, regardless of the practitioner’s personal reason. - If the dentist and the patient agree, the dentist may refer the patient to another provider who is
more willing or better suited (in keeping with the patient’s oral health status) to provide
treatment. - A patient who has been under the care of a dentist and then develops AIDS or a related condition
must be treated by that dentist or receive a referral that is satisfactory for and agreed to by the
patient. - The CDC and the American Dental Association recommend that infected dentists inform their
patients of their HIV serostatus and should receive consent or refrain from performing invasive
procedures.
Two major consideration in dental treatment for patients living with HIV/AIDS
- Current CD4+ lymphocyte count.
- Level of viral load.
Other: neutrophils, platelets.
Dental treatment of HIV-infected patients without symptoms is no different from that
provided for any other patient in the practice. Generally, this is true for patients with a
CD4+ cell count of more than –/μL
350
Patients who are symptomatic for the early stages of AIDS (i.e., CD4+ cell count
<—/μL) have increased susceptibility to opportunistic infections and may be
medicated with prophylactic drugs.
200
Patients with AIDS can receive almost any dental care needed and desired after the
possibility of significant (3) has
been ruled out
immunosuppression, neutropenia, or thrombocytopeniz
For invasive dental procedures (including scaling and curettage)
*
* Patients with CD4+ cell counts below 200/μL or severe neutropenia (neutrophil count
<500/μL):
in patients with severe thrombocytopenia
Medical consultation (adverse reactions with ART and/or current blood dyscrasias)
use prophylactic antibiotics;
special measures my be indicated (platelet replacement)
Treatment Planning Considerations
o In patients with periodontal disease whose general health status is not clear,
periodontal scaling for several teeth can be provided to allow assessment of tissue
response and bleeding. If no problems are noted, the rest of the mouth can be treated.
— may be required if the patient’s CD4+ cell count is
below 200/μL or if tissues remain — to routine therapy.
o — has good success in patients with HIV infection, and no
modifications are required.
Adjunctive antibacterial measures
unresponsive
Root canal therapy
Since the late 1980s to date, oral manifestations have been acknowledged to
represent a major component of HIV infection that can correlate with
treatment
responses and disease progression.
—-can present as an early clinical sign of HIV disease soon after
seroconversion alerting clinicians for further investigation in the appropriate
clinical scenario.
Oral lesions
Although it is unlikely to encounter many of the oral lesions associated with HIV
in general dental practice, oral healthcare providers should be familiar with
HIVrelated oral manifestations and comfortable in managing and referring patients
with HIV/AIDS.
Persistent generalized lymphadenopathy (PGL)
* After seroconversion, HIV disease often
remains silent except for —.
* The prevalence of this early clinical sign
varies; however, in several studies it
approaches —%.
* PGL consists of lymphadenopathy that
has been present for – months and
involves two or more extrainguinal sites.
* The most frequently involved sites are the
(4)
* Nodal enlargement usually is larger than – cm, and varies from — cm.
* Because lymphoma is known to occur in this population, a lymph node biopsy may be indicated
for localized or bulky —, when — is present, or when
requested for patient reassurance.
* PGL does warn of progression to —; almost — of affected and untreated patients will
have diagnostic features of — within – years
PGL
70
> 3
posterior and anterior cervical,
submandibular, occipital, and axillary
nodes.
1, 0.5 to 5.0
adenopathy, cytopenia or an elevated ESR,
AIDS, one-third, AIDS, 5
— is the most common intraoral manifestation of HIV infection and often is the
presenting sign that leads to the initial diagnosis.
Candidiasis
- The most common organism identified in oral candidiasis is —
Candida albicans.
Approximately one— of HIV-infected individuals and more than —% of patients with AIDS
develop oral candidiasis at some time during their disease course
third
90
types of oral candidiasis
(4)
- Pseudomembranous candidiasis (appears when the CD4+ lymphocyte count <200 cells/mm3)
- Erythematous candidiasis (appears when the CD4+ lymphocyte count <400 cells/mm3)
- Hyperplastic candidiasis
- Angular cheilitis
- — multifocal oral involvement is common in HIV-infected patients.
Chronic
Some studies have shown that development of candidiasis correlates more closely with viral load
than CD4+ cell count.
Oral candidiasis can be — and associated with a reduction in taste and smell, which may
lead to decreased food intake and further wasting.
painful
Oral Candidiasis
Treatment
* — often is ineffective.
* Topical — is effective but has high rate of recurrence.
* Systemic (2) are effective but have a number of drug interactions and
may result in drug-resistant candidiasis.
* If azoles fail, then IV — B can be administered. (nephrotoxicity)
Nystatin
clotrimazole
fluconazole and itraconazole
amphotericin
The most common EBV-related lesion in patients with
AIDS. (EBV is associated with several forms of lymphoma
in HIV-infected patients)
Oral hairy leukoplakia
The presence of OHL in HIV-infected patients is a sign of
severe immunosuppression and advanced disease
OHL also has been reported in transplant recipients, but its
presence in the absence of a known cause of
— strongly suggests HIV infection.
immunosuppression
OHL clinically presents as a
white mucosal plaque that does
not rub off. Most cases occur on the lateral border of the
tongue and range in appearance from faint, white vertical
streaks to thickened, furrowed areas of leukoplakia with a
shaggy surface.
The lesions infrequently may extend to cover the (5)
entire
dorsal and lateral surfaces of the tongue. Rarely, the buccal
mucosa, soft palate, pharynx, or esophagus may be
involved.
Oral hairy leukoplakia
Histology
* Thickened — (corrugated or thin projections)
* Epithelium is acanthotic and exhibits a bandlike zone of
lightly stained cells with abundant cytoplasm (“—”) in the upper spinous layer.
* Characteristic pattern of peripheral margination of
chromatin termed — caused by extensive EBV
replication that displaces the chromatin to the nuclear
margin.
* — is not noted.
* In a patient with known HIV infection, the clinical features
of OHL typically are sufficient for a presumptive diagnosis.
* When definitive diagnosis is necessary, demonstration of
EBV can be achieved by (5)
parakeratin
balloon cells
nuclear beading
Dysplasia
in situ hybridization, PCR,
immunohistochemistry (IHC), Southern blotting, or electron
microscopy.
Hyperpigmentation
Mucosal, cutaneous, and/or nail(s) hyperpigmentation may be induced by:
(4)
- A variety of drugs taken by HIV/AIDS patients such as zidovudine and emtricitabine-based HIV
regimens. - Drugs used to control microbial infections in these patients such as ketoconazole (fungalinfections), clofazimine (leprosy and some TB), and pyrimethamine (toxoplasmosis/antiparasitic).
- Destruction of the adrenal cortex by disseminated infections (e.g. deep fungal infections) in this
immunocompromised population is another possible cause of the observed hyperpigmentation. - Pigmentation with no apparent cause has arisen in HIV-infected patients, and some investigators
have theorized that this may be a direct result of HIV infection.
Hyperpigmentation
Tx (3)
- Usually, no treatment is indicated.
- Single lesions may have to be biopsied so that melanoma
can be ruled out. - Patients with adrenal insufficiency may require
corticosteroids.
Linear gingivitis
Periodontal & gingival disease
* Linear gingivitis appears with a distinctive linear band of erythema that involves the — and
extends — mm apically.
* The alveolar mucosa and gingiva may demonstrate — in a significant percentage of
cases.
* This diagnosis should be reserved for gingivitis that does not respond to improved — and exhibits a
greater degree of — than would be expected for the amount of plaque present
* Results from an abnormal host immune response to subgingival bacteria or may represent an unusual pattern of —
free gingival margin
2 to 3
punctate or diffuse erythema
plaque control
erythema
candidiasis
- Necrotizing ulcerative gingivitis (NUG) appears as..
- Patients with NUG have (4)
ulceration and necrosis of one or more
interdental papillae with no periodontal attachment loss.
interproximal gingival necrosis, bleeding, pain, and halitosis.
Necrotizing ulcerative periodontitis (NUP) is characterized by
gingival ulceration and necrosis associated with
rapidly progressing loss of periodontal attachment. (Attachment loss of more than 6 mm within a 6-month period
is not unusual)
Although severe cases can affect all teeth,
multiple isolated defects often are seen and contrast with the diffuse
pattern associated with typical chronic periodontitis
*(3) are common.
Edema, severe pain, and spontaneous hemorrhage
Deep pocketing usually is not seen because
extensive gingival necrosis typically coincides with loss of the adjacent
alveolar bone.
Necrotizing stomatitis may be seen as an extension of
NUP or may involve oral mucosa separate from the
gingiva. (biopsy in this case is indicated)
Necrotizing stomatitis
* Involves predominantly soft tissue or extend into the underlying bone, resulting in
extensive sequestration.
Linear gingivitis may be treated with (4)
débridement, povidone-iodine irrigation, chlorhexidine
mouth rinse, and/or antifungal medication.
The treatment of NUG and NUP revolves around (5)
débridement, antimicrobial therapy, pain
management, immediate follow-up care, and long-term maintenance.
- The initial removal of necrotic tissue typically is combined with —
- The use of systemic antibiotics usually is not necessary, but — (narrow spectrum to
suppress periodontal pathogens without strongly promoting candidal overgrowth) has been
administered to patients with extensive involvement and severe acute pain. - All patients should use — mouth rinses initially and for long-term maintenance.
- After initial débridement, removal of additional diseased tissue should be performed within — hours and again every — days for two to three appointments, depending on the patient’s response. At this point, monthly recalls are necessary until the process stabilizes; evaluations then
are performed every — months.
povidone-iodine irrigation.
metronidazole
chlorhexidine
24, 7-10, 3
Patients may demonstrate conventional gingivitis, chronic periodontitis, and progressive nonnecrotizing periodontitis.
* In these cases,
periodontal attachment loss can be combated successfully with regular professional
scaling and root planing, plus optimization of oral hygiene. Patients should be encouraged to
discontinue their tobacco habit.
The prevalence of oral recurrent HSV infection among HIV-infected individuals increases significantly
once the CD4+ cell count < —/mm 3.
50
Within the setting of HIV infection, recurrent herpetic lesions may be widespread, occur in
an atypical
pattern, and persist for months.
- Herpes labialis may extend to the facial skin and exhibit extensive — spread.
lateral
Persistence of active HSV infection for more than — month in a patient infected with HIV is one
accepted definition of AIDS
1
Evaluation for — should be performed on all persistent
oral ulcerations in HIV-infected individuals.
HSV
- Investigators have discovered HSV in 10% to 19% of such
cases (with an additional 10% to 28% exhibiting coinfection
by HSV and CMV).
HSV
* Systemic acyclovir, valacyclovir, or famciclovir for at least – days can be effective. Higher doses may be needed during
severe immunosuppression.
* An elixir or syrup of diphenhydramine (Benadryl) of — mg/5 mL can be used for pain control.
5
12.5
Varicella-zoster virus lesions
* Among patients with HIV infection, herpes zoster is often —, with increased morbidity and mortality
rates.
* Many of these patients are younger than — years, in contrast to immunocompetent patients who typically
develop herpes zoster later in life.
severe
40
Varicella-zoster virus lesions
* In patients with well-controlled HIV disease, herpes zoster
usually is confined to a ..
* In full-blown AIDS, dissemination to ..
is not unusual.
single dermatome but persists longer
than usual.
multiple dermatomes
Varicella-zoster virus lesions
Severe intraoral involvement may lead to
bone
sequestration and loss of teeth; these sequelae may be
delayed a month or more after the initial onset of herpes
zoster.
Varicella-zoster virus lesions
* Associated pain typically is intense.
Tx (3)
- Valacyclovir 1 g PO tid; famciclovir 500 mg PO tid; acyclovir 800 mg PO 5 times per day.
- IV acyclovir may be needed for severe herpes zoster in patients with immunosuppression.
- Routine zoster vaccination for HIV-infected patients is not recommended currently; however, according
to some experts, zoster vaccination may be considered for those with well-controlled HIV disease and
CD4+ cell counts > 200/ mm 3 .
T
HIV-related salivary gland disease
HIV-associated salivary gland disease can arise anytime during HIV infection and is considered a
localized manifestation of
diffuse infiltrative lymphocytosis syndrome (DILS).
HIV-related salivary gland disease
DILS is characterized by
CD8+ lymphocytosis with diffuse lymphocytic infiltration of various sit
HIV-related salivary gland disease
The etiopathogenesis is unknown, although some investigators hypothesize that … may play a role.
autoimmune
dysregulation and underlying viral opportunistic infection (e.g., with EBV)
HIV-related salivary gland disease
The main clinical sign is —, particularly affecting the parotid. — involvement is seen in about 60% of cases and often is associated with cervical lymphadenopathy
salivary gland enlargement
Bilateral
HIV-related salivary gland disease
* — is a variable finding.
Xerostomia
HIV-related salivary gland disease
Microscopic changes within the affected
glands may include
lymphocytic infiltration,
hyperplasia of intraparotid lymph nodes, and,
in long-standing cases, lymphoepithelial cyst
formation.
HIV-related salivary gland disease
The most widely accepted treatments for DILS
are (2),
although some patients have been treated with
surgery or radiation therapy.
oral prednisone and antiretroviral therapy
HIV-related salivary gland disease
Most investigators have noted regression after initiation of ART, whereas others have reported an
increased prevalence with ART, possibly due to —.
IRS
Recurrent aphthous stomatitis (RAS)
* Most lesions are of the more uncommon forms— (2)
* With more severe reduction of CD4+ cell count, –
lesions become more prevalent.
* Lesions that are — or that do not
respond to treatment should be biopsied.
* Treatment of persistent lesions involves potent —. Systemic steroids generally
are avoided to prevent further immunosuppression.
major and herpetiform.
major
chronic or atypical
topical or
intralesional corticosteroids
HIV-related (non-specific) oral ulceration
* The EC-Clearinghouse-WHO cohorts (1993) defined oral
ulceration in the context of HIV as a
distinct entity not
corresponding to any pattern (minor, major, or
herpetiform) of recurrent aphthous stomatitis (RAS) nor
caused by fungal, bacterial, or viral organisms
Antiretroviral therapy induced-oral ulceration
- Ulcerations induced by ART has also been reported.
Human papillomavirus (HPV) infections
Among HIV-infected individuals, most HPV lesions arise in
the — region, although oral involvement also is
possible.
anogenital
skipped
Human papillomavirus (HPV) infections
Benign HPV lesions:(4)
Oral squamous papilloma, verruca
vulgaris, condyloma acuminatum, and multifocal epithelial
hyperplasia.
Human papillomavirus (HPV) infections
The prevalence of these oral HPV lesions in HIV-infected
patients is greater than that observed among
— individuals.
immunocompetent
Human papillomavirus (HPV) infections
Unusual HPV types (such as, HPV– [associated with butcher’s
warts], HPV—, and HPV— [associated with multifocal
epithelial hyperplasia]) frequently are identified in oral HPV
lesions arising in HIV-infected patients.
7
13
32
Human papillomavirus (HPV) infections
The (4) are
most frequently involved.
labial mucosa, tongue, buccal mucosa, and gingiva
Human papillomavirus (HPV) infections
The lesions may exhibit a cluster of
sessile papules.
white, spikelike
projections, pink cauliflower-like growths, or slightly elevated
Human papillomavirus (HPV) infections
Histopathology
* Lesions may be sessile or papillary and
covered by acanthotic or hyperplastic
stratified squamous epithelium
* The affected epithelium often
demonstrates vacuolization of numerous
epithelial cells (i.e., —) and
occasionally may exhibit mild variation in
nuclear size.
* — has been noted within HPVrelated lesions in patients with AIDS
and mandates close observation for
development of —
Oral mucosa exhibiting extensive koilocytosis
in the superficial spinous cell layer.
koilocytosis
Dysplasia
squamous cell
carcinoma.
Human papillomavirus (HPV) infections
Treatment
* — is the most commonly used treatment for oral HPV
lesions; additional surgical options include cryosurgery, electrocautery, and
laser ablation.
* All of these surgical methods are associated with frequent —.
* — may expose the surgical team and patient
to a plume containing infectious HPV.
Surgical excision
recurrence
Electrocautery and laser ablation
Lymphoma
The marked reduction in CD4+ T-helper lymphocytes, to a great degree, explains the lack of an effective
immune response seen in patients with AIDS and contributes to the increase in malignant disease that has
been found to be associated with AIDS, including (3)
Kaposi sarcoma, lymphoma, and carcinomas.
Lymphoma
—currently represents the most common malignancy among the AIDS
population in the United States.
Non-Hodgkin lymphoma (NHL)
Lymphoma
Most cases represent high-grade, aggressive B-cell neoplasms.
May be associated with —
EBV and/or HHV-8.
Lymphoma
Lymphoma in patients with AIDS usually occurs in —
locations
extranodal
Lymphoma
Oral lesions are seen in approximately 4% of patients with
AIDS-related NHL and most frequently involve the (3)
gingiva,
palate, and tongue.
Lymphoma
Intraosseous involvement also has been documented and may
resemble diffuse progressive periodontitis with loss of
periodontal attachment and loosening of teeth. In these cases, (2) may represent radiographic clues to the diagnosis.
widening of the periodontal ligament and loss of lamina dura
Lymphoma
With the inclusion of —, lymphoma survival for the HIVinfected population often approaches that for the general
population.
ART
Kaposi sarcoma
The lesion most likely arises from
endothelial cells, which may express markers for both lymphatic and
blood vessel differentiation and is caused by human herpesvirus 8 (HHV-8).
Kaposi sarcoma
Four clinical presentations are
recognized:
- Classic
- Endemic (African)
- Iatrogenic (transplant-associated)
- Epidemic (AIDS-related)
Kaposi sarcoma currently represents the
— most common malignancy
among people with AIDS in the United
States.
second
Kaposi sarcoma typically evolves through three stages:
- Patch (macular) 2. Plaque 3. Nodular
Kaposi sarcoma
In Western countries, Kaposi sarcoma has been reported primarily in HIV-infected, adult, male
homosexuals and is thought to be related to
sexual transmission of HHV-8.
Kaposi sarcoma
In — both AIDS-related and
endemic types of Kaposi sarcoma
frequently are seen, with no gender
predilection and a significant number
of children affected
Africa
Kaposi sarcoma
Infection before — activity
suggests alternate transmission
pathways
sexual
Kaposi sarcoma
Relatively high titers of HHV-8 have
been found in —, and HHV-8
exhibits tropism for oral and
oropharyngeal epithelial cells
saliva
Kaposi sarcoma
A — is required for definitive
diagnosis, although a presumptive
clinical diagnosis sometimes is made.
biopsy
Kaposi sarcoma
Other lesions can have a similar
clinical appearance in HIV-infected
patients, including (2)
bacillary
angiomatosis and lymphoma.
Relative to the general population, HIV-infected individuals have an estimated twofold increased risk of
developing
oral cavity and pharyngeal cancer.
Studies of various HIV/AIDS cohorts have demonstrated a high prevalence of known risk factors for
oral and pharyngeal cancers (e.g., tobacco use and HPV infection).
Oral squamous cell carcinoma tends to occur at a — age among HIV-infected individuals than
non-HIV-infected individuals
younger
Treatment also is not significantly different for HIV-infected patients and consists of (3)
surgical resection,
radiation therapy, and/or chemotherapy.
Most HIV-infected patients with a diagnosis of oral squamous cell carcinoma have advanced disease
and an — prognosis
unfavorable
Oral squamous cell carcinoma
Clinical DDX:
(4)
- SCC
- Deep fungal infection
- Tuberculosis
- Atypical
lymphoproliferative
disorder
