DENTAL CONSIDERATIONS IN HIV AND HEPATITIS

OVERVIEW OF HIV INFECTION

Although the cause was unknown at the time, problems associated with the human
immunodeficiency virus (HIV) were first noted in the United States in mid-1981 when the deaths
of several young men living in metropolitan centers were reported to the Centers for Disease
Control and Prevention (CDC). This syndrome of infection, immune suppression, and
opportunistic diseases (infections and neoplasm’s) eventually became known as the acquired
immune deficiency syndrome (AIDS) (CDC, 1992). Since 1981, HIV infection has become
pandemic with over 30 million people infected
In 1984 three independent laboratories identified the causative agent. A French team
from the Pasteur Institute identified a retrovirus termed the lymphadenopathy-associated virus
(LAV) and reported it as the causative agent for AIDS. In the United States, a team from the
National Institutes of Health isolated a retrovirus, identified as the human T lymphotropic virus
III (HTLV-III) and labeled it as the etiologic agent for AIDS. A team in San Francisco also
isolated a retrovirus, AIDS-related virus (ARV), and designated it as the causative agent for
AIDS. All were similar retroviruses, with minor differences in amino acid sequences. In 1986,
the World Health Organization recommended that the virus be called the human
immunodeficiency virus.
HIV is transmitted by sexual means, through the exchange of body fluids (especially infected
semen during intercourse); by non-sexual means, via the parenteral transfer of infected blood; or
through vertical transmission to infants born of infected mothers. The only fluids that have been
demonstrated to be associated with transmission of the virus are blood, semen, breast milk, and
vaginal secretions. Casual contact (shaking hands, hugging, casual kissing, etc.) has not been
shown to transmit HIV. Individuals who appear to be most susceptible to HIV infection are those
with repeated exposures to the virus, other concurrent sexually transmitted infections (STIs), and
immune systems that have been challenged by repeated exposures to various antigens (semen,
hepatitis B, or blood products). According to the CDC, of all AIDS cases reported by September
2001, sexual behavior was the most common route of transmission with heterosexual
transmission the most common means of transmission to women; 82% of cases have been in
adult and adolescent men, and18% have been in adult and adolescent women.

REDUCING THE POTENTIAL FOR DISEASE TRANSMISSION IN THE DENTAL OFFICE

A major concern for any clinician treating HIV-infected patients is to minimize the risk
of exposure for themselves, their staff, and other patients. Dental procedures frequently cause
bleeding and exposure to infected blood is a known means of HIV transmission. Saliva has not
been shown to transmit HIV in a dental setting, but the potential for exposure to bloody saliva
does exist. To reduce the risk of disease transmission, the American Dental Association (ADA),
the Occupational Safety and Health Association (OSHA), and the CDC have set standards of
infection control for dental health care personnel (DHCP).
Infectious organisms can be spread through several routes in the dental office: direct skin
or percutaneous exposure to blood, oral fluids, or other secretions; indirect contact with
contaminated instruments, operatory equipment or environmental surfaces; and/or contact with
airborne contaminants present in either droplet spatter or aerosols of oral and respiratory fluids.
Infection via any of these routes requires that all of the following conditions be present
(commonly referred to as “the chain of infection”): a susceptible host; a pathogen with sufficient
infectivity and numbers to cause infection; and a portal through which the pathogen may enter
the host. Effective infection control strategies are intended to break one or more of these “links”
in the chain, thereby preventing infection. HIV can be transmitted through sharps injuries or
direct contact with open wounds on the skin or mucous membranes. There is no evidence that
HIV is transmitted via the airborne route or insect vectors. Because individuals with an
infectious disease cannot always be identified through history review or physical examination,
the CDC recommends that DHCP follow a standard set of precautions for all patients at all times.
The use of these precautions has reduced the chance that an infection can be transmitted in the
dental operatory. Standard precaution procedures are widely publicized and describe techniques
used to reduce contact with organisms (breaking the chain at the portal of entry) and the potential
transmission of infectious agents. These precautions protect DHCP from all blood borne
organisms, including HIV.
DHCP must wear protective devices designed to protect personnel and patients in dental-care
settings. Medical gloves (latex or vinyl) must be worn when there is any potential for coming
into contact with blood, blood contaminated saliva, or mucous membranes. Nonsterile gloves are
appropriate for examinations and other non-surgical procedures; sterile gloves should be used for
surgical procedures. Before treatment of each patient, DHCP should wash their hands and put on
new gloves; after treatment or before leaving the dental operatory, DHCP should remove and
discard gloves, then wash their hands. DHCP always should wash their hands and reglove
between patients. Chin length plastic face shields or surgical masks and protective eyewear
should be worn when splashing or spattering of blood or other body fluids is likely, as is
common in dentistry. Masks should be changed between patients or when wet or soiled. Eyewear
should be washed with an appropriate cleaning agent and, when visibly soiled, disinfected
between patients.
Protective clothing (reusable or disposable gowns, laboratory coats, or uniforms) should be worn
when clothing is likely to be soiled with blood or other body fluids. Reusable protective clothing
should be washed, using a normal laundry cycle, according to the instructions of detergent and
machine manufacturers. Protective clothing should be changed at least daily or as soon as it
becomes visibly soiled. Impervious-backed paper, aluminum foil, or plastic covers should be
used to protect items and surfaces (e.g., light handles or x-ray unit heads) that may become
contaminated by blood or saliva during use and that are difficult or impossible to clean and
disinfect. These coverings should be discarded and replaced between patients. These precautions
significantly reduce the risk of exposure to HIV when used consistently and correctly.
Unfortunately, humans are not perfect and accidents can happen. Should a blood exposure occur,
the CDC has developed guidelines for post-exposure prophylaxis (PEP).

IMPLICATIONS FOR ORAL HEALTH CARE PROVIDERS

Oral manifestations of HIV are common and may be the first clinical features of the
disease noted by the patient and/or health care provider. Because the DHCP may be the first to
recognize the signs and symptoms of HIV, each provider must be adept at taking a
medical/dental history, examining the oral cavity and surrounding tissues for signs of disease,
and recognizing when an abnormality is present.
 Effective treatment plans cannot be developed without a definitive diagnosis for the
abnormalities discovered. Proper diagnosis and treatment have been shown to reduce the
morbidity associated with HIV infection and to increase the life span of the infected individual.
Dental practitioners should understand the relevance of the comprehensive dental exam in
relation to the detection of HIV infection. A thorough head and neck examination must be
performed. Any pathologic conditions that are found should be evaluated comprehensively and
not in isolation from other oral health problems. A proper dental examination is of critical
importance because many physicians do not perform thorough intraoral examinations at routine
visits. It is the responsibility of the dental practitioner to screen for oral cancer and intraoral
lesions that may be indicative of HIV, oral disease, or oral/perioral signs of other systemic
diseases.

ORAL MANIFESTATIONS OF HIV

Dental expertise is necessary for proper management of oral complications in HIV
infection or AIDS. Medical clinicians should be able to recognize HIV-associated oral disease
and to provide appropriate care and referral. Factors that predispose to HIV-related oral
conditions include CD4+ cell count of less than 200/μL, plasma HIVRNA levels greater than
3000 copies/mL, xerostomia, poor oral hygiene, and smoking. For individuals with unknown
HIV status, oral manifestations may suggest possible HIV infection, although they are not
diagnostic of infection. For persons living with HIV disease who are not yet on therapy, the
presence of certain oral manifestations may signal progression of HIV disease. For patients on
antiretroviral therapy, the presence of certain oral manifestations may signal an increase in the
plasma HIV-1 RNA level. HIV-related oral abnormalities are present in 30% to 80% of HIV-
infected individuals, and these abnormalities are often inaccurately described in medical care.
The overall prevalence of oral manifestations of HIV disease has changed since the
advent of potent antiretroviral therapy. One study by Patton and colleagues noted a reduction of
oral lesions from 47.6% pre-potent antiretroviral therapy to 37.5% during the potent
antiretroviral therapy era (Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2000). Overall,
there appears to be a reduced incidence of candidiasis, Kaposi’s sarcoma, oral hairy leukoplakia,
and necrotizing ulcerative periodontitis; an increased incidence of salivary gland disease, oral
warts, and dental caries in the form of “brittle teeth syndrome;” and a relatively unchanged
incidence of oral ulcers. Some of the oral conditions encountered in HIV-infected individuals are
discussed below.

Xerostomia
Xerostomia is a major contributing factor in dental decay in HIV-infected individuals.
More than 400 medications lead to symptoms of xerostomia. Approximately 30% to 40% of
HIVinfected individuals experience moderate to severe xerostomia in association with the effects
of medications (eg, didanosine) or the proliferation of CD8+ cells in the major salivary glands.
Changes in the quantity and quality of saliva, including diminished antimicrobial properties, lead
to rapidly advancing dental decay and periodontal disease. Use of crystal methamphetamine is
associated with increased risk of HIV acquisition, and its use by infected individuals can be
associated with rapid dental decay known as “meth mouth”. The primary factor in this condition
is probably xerostomia, with contributions from bruxism, poor diet, sugar cravings, and the
corrosive constituents of crystal methamphetamine— ie, lithium, muriatic and sulfuric acids, and
lye.

Candidiasis
The 3 common presentations of oral candidiasis are angular cheilitis, erythematous
candidiasis, and pseudomembranous candidiasis. Angular cheilitis presents as erythema or
fissuring of the corners of the mouth. It can occur with or without erythematous or
pseudomembranous candidiasis, and can persist for an extensive period of time if left untreated.
Treatment involves the use of a topical antifungal cream applied directly to the affected areas 4
times a day for 2-week treatment period.
Erythematous candidiasis may be the most under diagnosed and misdiagnosed oral
manifestation of HIV disease. The condition presents as a red, flat, subtle lesion on the dorsal
surface of the tongue or on the hard or soft palates. It may present as a “kissing” lesion—if a
lesion is present on the tongue, the palate should be examined for a matching lesion, and vice
versa. The condition tends to be symptomatic, with patients complaining of oral burning, most
frequently while eating salty or spicy foods or drinking acidic beverages. Clinical diagnosis is
based on appearance, as well as on the patient’s medical history and virologic status. The
presence of fungal hyphae or, more likely, blastospores can be confirmed by performing a
potassium hydroxide (KOH) preparation. Pseudomembranous candidiasis (or thrush) appears as
creamy, white, curd like plaques on the buccal mucosa, tongue, and other oral mucosal surfaces.
The plaques can be wiped away, typically leaving a red or bleeding underlying surface. The most
common organism involved is Candida albicans; however, there are increasing reports of
involvement of non-albicans species.
Topical treatments for mild to moderate cases of both erythematous and
pseudomembranous candidiasis include clotrimazole troches, nystatin oral suspension, and
nystatin pastilles. It should be noted that the common nystatin oral suspension contains 50%
sucrose, which is cariogenic; this is less of a potential problem if fluoride is prescribed along
with the nystatin. The clotrimazole oral treatment is formulated with fructose, which is less
cariogenic. Systemic agents for moderate to severe disease consist of fluconazole, the most
widely used drug; itraconazole; and voriconazole, the latter of which should be reserved for
cases of fluconazole resistance.
Factors associated with azole-resistant disease include prior exposure to azoles, low
CD4+ cell count, and presence of non-albicans species. The primary lesson to be learned in the
treatment of any candidiasis— whether it be with a topical agent for mild to moderate disease or
a systemic agent for more severe disease—is that treatment must be continued for at least 2
weeks in order to reduce organism colony-forming units to levels low enough to prevent
recurrence.

Oral Hairy Leukoplakia

Oral hairy leukoplakia, which is caused by Epstein-Barr virus, presents as a white,
corrugated lesion on the lateral borders of the tongue; the lesion cannot be wiped away. There
has been a marked decrease in the incidence of oral hairy leukoplakia in the potent antiretroviral
era. This condition is normally asymptomatic and does not require therapy unless there are
cosmetic concerns. However, it is important to note that the condition is observed with immune
deterioration and that patients presenting with it while on antiretroviral therapy may thus be
experiencing failure of their current regimen.
Periodontal Disease
Linear gingival erythema
Linear gingival erythema, or “red band gingivitis,” presents as a red band along the
gingival margin and may or may not be accompanied by occasional bleeding and discomfort. It
is seen most frequently in association with anterior teeth, but commonly extends to the posterior
teeth. It can also present on attached and non-attached gingiva as petechia like patches. Some
data indicate a relationship between sub-gingival colonization of Candida species and HIV-
related periodontal conditions including linear gingival erythema. The most recent American
Academy of Periodontology classification of periodontal diseases groups linear gingival
erythema under “gingival disease of fungal origin.” However, antifungals typically are not
needed for treatment. Treatment includes debridement by a dental professional; twice-daily
rinses with a 0.12% chlorhexidine gluconate suspension for 2 weeks, and improved home oral
hygiene.

Necrotizing Ulcerative Periodontitis

Although necrotizing gingivitis and necrotizing periodontitis may reflect the same disease
entity, they are differentiated by the rapid destruction of soft tissue in the former condition and
hard tissue in the latter. Necrotizing ulcerative periodontitis is a marker of severe immune
suppression. The condition is characterized by severe pain, loosening of teeth, bleeding, fetid
odor, ulcerated gingival papillae, and rapid loss of bone and soft tissue. Patients often refer to the
pain as “deep jaw pain.” Treatment includes removal of dental plaque, calculus, and necrotic soft
tissues utilizing a 0.12% chlorhexidine gluconate or 10% povidone-iodine lavage, and institution
of antibiotic therapy. Pain management is crucial, as is attention to nutrition in these patients.
Timely referral to primary care is indicated to rule out other systemic opportunistic infections.

Kaposi’s Sarcoma
Kaposi’s sarcoma is still the most frequent HIV-associated oral malignancy, although its
incidence has dramatically decreased in the potent antiretroviral therapy era. Kaposi’s sarcoma-
associated herpes virus (KSHV) has been identified as the etiologic agent. Kaposi’s sarcoma can
be macular, nodular, or raised and ulcerated, with color ranging from red to purple; early lesions
tend to be flat, red, and asymptomatic, with the color becoming darker as the lesion ages.
Diagnosis is frequently missed in African-American patients due to lesion coloration.
Progressing lesions can interfere with the normal functions of the oral cavity and become
symptomatic secondary to trauma or infection. Definitive diagnosis requires biopsy. Treatment
ranges from localized injections of chemotherapeutic agents, such as vinblastine sulfate, to
surgical removal. Oral hygiene must be stressed. Systemic chemotherapy may be the treatment
of choice for patients with extraoral and intraoral Kaposi’s sarcoma.

Oral Warts—Human PapillomaVirus

The incidence of oral warts due to human papillomavirus (HPV) has dramatically
increased in the potent antiretroviral therapy era. Studies indicate that the risk of HPV-associated
oral warts is associated with a 1-log10 or greater decrease in plasma HIV RNA level within the 6
months prior to oral HPV diagnosis, suggesting that the development of warts may be related to
immune reconstitution. The warts may be cauliflower-like, spiked, or raised with a flat surface.
Treatment may involve surgery, laser surgery, or cryotherapy. It should be noted that HPV
survives in aerosol. Topical 5-fluorouracil treatment has been used on external lesions. It should
be noted, however, that this is a specialized treatment and should only be used by those
experienced with the use of this topical medication. Lesions tend to recur after treatment.

Ulcerative Diseases
Herpes simplex virus
Herpes simplex virus (HSV)-1 infection is widespread and oral lesions are common.
Recurrent intraoral HSV outbreaks start as a small crop of vesicles that rupture to produce small,
painful ulcerations that may coalesce. Lesions on the lip are fairly easy to recognize. In the
mouth, lesions on keratinized, or fixed, tissues, including the hard palate and gums, should
prompt suspicion of HSV infection. Herpetic ulcerations are often self-limiting, although the use
of an antiviral medication such as acyclovir is sometimes necessary to control the outbreak.

Aphthous ulcerations
Recurrent aphthous ulcerations appear on non-keratinized, or non-fixed, tissues, such as
the labial or buccal mucosa, floor of the mouth, ventral surface of the tongue, posterior
oropharynx, and maxillary and mandibular vestibules. Their cause is unknown. The lesions are
characterized by a halo of inflammation and a yellow-gray pseudomembranous covering. They
are very painful, especially during consumption of salty, spicy, or acidic foods and beverages, or
hard or rough foods. In immunocompromised patients, these lesions tend to persist for longer
than the 7- to 14- day period observed in immunocompetent individuals. Treatment for milder
cases involves the use of topical corticosteroids such as dexamethasone elixir (0.5 mg/5 mL) 5
mL swished for 1 minute and then expectorated, 2 to 3 times daily until symptoms resolve. For
more severe occurrences, systemic corticosteroids such as prednisone are used.

Neutropenic ulcerations
Neutropenic ulcerations are very painful ulcerations that can appear on both keratinized
and non-keratinized tissues, and are associated with absolute granulocyte counts of less than
800/μL. These lesions are being found with increasing frequency in the HIV-infected population,
although the cause of this increase in frequency remains unknown. Large, unusual looking, or
fulminant ulcers in the oral cavity that cannot otherwise be identified or explained should prompt
suspicion of this condition. Patients should receive granulocyte colony-stimulating factor
treatment prior to systemic or topical steroid treatment, depending on the size and location of the
lesion.

Pain in ulcerative disease

Pain management is a crucial component of treating ulcerative oral diseases. Pain usually
is treated with topical anesthetics or systemic analgesics. However, relief provided by topical
anesthetics is usually of short duration. Furthermore, anesthetic mouth rinses numb the taste
buds, resulting in a decreased desire to eat, and diminished nutritional intake can have a
significant negative impact on overall well-being for many patients. Systemic analgesics are also
somewhat effective, but do not specifically address localized pain. One product that has been
found to be effective in ulcer pain control is a rinse composed of polyvinylpyrrolidone,
hyaluronic acid, and glycyrrhetinic acid. If other topical treatments are to be used (eg, topical
steroids), they should be applied prior to use of this rinse, since the barrier formed by the product
will prevent penetration of the other topical medications.
TESTING FOR HIV INFECTION
A variety of antibody tests are used to screen for HIV infection. Table 3 describes the screening
process that must be accompanied by pre- and posttest counseling. Tests are available from
primary care clinicians, health care plans, and most local health departments. When a patient has
limited options for health care or is fearful of being tested by her physician, the health
department is a good referral.
Rapid tests. Rapid HIV screening tests, first approved in 1996, can be performed in an average
of 10 minutes. In terms of time and convenience, these tests offer dramatic improvements over
standard antibody tests that require days or even weeks for results. Most significantly,
individuals with negative test results do not have to return for a second visit to obtain their test
results; they receive them shortly after the test is performed. For positive tests, however, a
confirmatory EIA and Western blot protocol is still required to eliminate false positives. This
requires a time delay and a second visit or appointment to obtain the results. Rapid test
methodologies include “dot blot” or “immunoblot” assays that produce a colored dot on the solid
phase surface, with or without an anti-human immunoglobulin control. Dipstick assays are also
available. The results of a number of studies confirm that the accuracy of rapid tests is similar to
standard ELISA screening protocols. Rapid tests are simple to perform and can be used in a wide
variety of settings. Because of this, they are likely to be used with increasing frequency in many
settings, including emergency rooms, indigent clinics, “point of care” testing, and in testing
situations where time is critical.

HIV Antibody Test Screening Process

The following steps are used in the process of testing blood for antibodies to HIV:
1. A highly sensitive enzyme immunoassay (EIA, ELISA) is done to detect serum antibodies that
bind to HIV antigens on test plates. Blood samples that are negative on this test are reported as
negative.
2. If the blood is EIA reactive, the test is repeated.
3. If the blood is repeatedly EIA reactive, a more specific confirming test, such as the Western
blot (WB) or immunofluorescence assay (IFA), is done.
• WB testing uses purified HIV antigens electrophoresed on gels. These are incubated with
serum samples. If antibody in the serum is present, it can be detected. The CDC and the
Association of State and Territorial Public Health Laboratory Directors define a positive Western
blot assay as any two of three bands (p24, gp41, gp 120/160) that correspond to HIV markers
present in the specimen. The criteria for a negative Western blot interpretation specify the total
absence of bands. All other band patterns are regarded as indeterminate, i.e., bands are present
but they do not fulfill diagnostic criteria.
• IFA is used to identify HIV in infected cells. Blood is treated with a fluorescent antibody
against p17 or p24 antigen and then examined using a fluorescent microscope.
4. Blood that is reactive in all of the first three steps is reported as HIV-antibody positive. The
combination of EIA and Western blot assay has an extremely high positive predictive value
(persons with positive tests are very likely to be infected), even in low-risk populations.
5. If the results are indeterminant, the following steps need to be taken:
• If in-depth risk assessment reveals that the individual does not have a history of high risk
activities: reassure the client that s/he is extremely unlikely to be infected with HIV and suggest
re-testing in 3 months.
• If in-depth risk assessment reveals that the individual does have a history of high risk activities:
Repeat antibody test at 1, 2, and 6 months; discuss harm reduction measures to protect partners
from infection; consider tests for HIV antigen detection.

When can HIV antibodies be detected? The “window period” is a critical concept in HIV
testing. The window period is the time between initial infection with HIV and the development
of enough antibodies to be detected through testing. In general, 3 to 12 weeks is required after
infection. A recently infected individual, therefore, may not test positive for HIV but could still
transmit HIV to others. The virus is not latent during the window period or any subsequent
period. In fact, the viral load is higher after initial infection than any period until advanced HIV
disease. After this initial “spike,” the viral load decreases to a more stable “set point.”
Understanding the window period is important for recommendations regarding further testing
and for risk prevention. A recently exposed person should be advised to return for HIV antibody
testing 6 weeks and 3 months after the exposure incident. Persons concerned about risk or
potential exposure should be counseled to take precautions to prevent transmission of HIV
during the window period. It is important to ensure that persons receiving pre- and post-HIV test
counseling understand the window period concept.
Hepatitis B and C infection: Clinical implications in dental practice

The liver has a broad range of functions in maintaining homeostasis and health. It
synthesizes the most essential serum proteins (albumin, transporter proteins, blood coagulation
factors V, VII, IX, and X, prothrombin, and fibrinogen, as well as many hormone and growth
factors), produces bile and its transporters (bile acids, cholesterol, lecithin, phospholipids),
intervenes in the regulation of nutrients (glucose, glycogen, lipids, cholesterol, amino acids), and
metabolizes and conjugates lipophilic compounds (bilirubin, cations, drugs) to facilitate their
excretion in bile or urine. Liver dysfunction alters the metabolism of carbohydrates, lipids,
proteins, drugs, bilirubin, and hormones. Accordingly, liver disease is characterized by a series
of aspects that must be taken into account in the context of medical and dental care. Hepatitis B
virus (HBV) is a DNA virus and one of many unrelated viruses that cause viral hepatitis. The
disease was originally known as “serum hepatitis”. Hepatitis C is a hepatotropic viral infection
caused by hepatitis C virus (HCV), which is a major cause of acute hepatitis and chronic liver
disease. It is characterized by inflammation of the liver and in many cases permanent damage to
liver tissue. The most common types of hepatitis are hepatitis A, B, C, D, E, and G. Hepatitis B
and C can lead to permanent liver damage and in many cases death. There are more than 2
billion people worldwide having evidence of recent or past HBV infection and 350 million are
chronic carriers. In the Southeast Asia region, there are estimated 80 million HBV carriers (about
6% of the total population). India has the intermediate endemic city of hepatitis B, with hepatitis
B surface antigen prevalence between 2% and 10% among the population studied. The number
of carriers in India has been estimated to be over 40 million. HBV and HCV infections are
serious public health problems that can have consequences in terms of psychological and
occupational diseases. HBV and HCV are common causes of occupational diseases transmitted
from patients to health care workers (HCWs) and vice versa, and also to HCWs’ families. It has
been estimated that 14.4% and 1.4% of hospital workers are infected with HBV and HCV,
respectively. Physicians, dentists, nurses, laboratory staff, and dialysis center personnel are at
high risk of acquiring infection. HCV prevalence varies widely among countries, with the
highest being in several African and eastern Mediterranean countries. The frequency of exposure
to HBV was the highest among dental healthcare workers according to a study conducted in
Japan. In another study, nurses were most commonly exposed to infection (41%), followed by
physicians (31%) among healthcare workers. Prevention of hepatitis B and C transmission
through the medical care setting is an important public health issue. Even after the introduction
of many programs and strategies, hepatitis infection continues to remain a health problem in
dental settings. Therefore, the present study considers aspects such as common oral
manifestations of hepatitis B and C infection for the clinician to be able to appropriately
diagnose, prevent, and manage the transmission and progression of this fatal disease.
The virus and its transmission
HBV is a DNA virus belonging to the family Hepadnaviridae. It is a complex 42 nm
double shelled particle. The outer surface or envelop of the virus contains hepatits B surface
antigen (HbsAg). It encloses an inner icosahedral 27 nm nucleocapsid (core), which contains
hepatitis B core antigen (Hbc Ag). Inside the core, there is a circular double stranded DNA and a
DNA polymerase.
Hepatits C virus is a RNA virus belonging to family Flaviviridae. Genetically distinct
viral groups have evolved with 9 different genotypes of hepatitis C and 40 different subgroups.
The sources of contagion include blood transfusion, percutaneous exposure through
contaminated instruments, and occupational exposure to blood. The individuals at the greatest
risk are hemophiliacs, patients on dialysis, and parenteral drug abusers. Other transmission
routes are sexual contact and the perinatal and idiopathic routes.

Clinical presentation of the disease

Around 30-50% of adults and children develop clinical illness typical of hepatitis B after
initial exposure to HBV. The incubation period for hepatitis B usually ranges from 60 to 150
days. Early symptoms that occur before jaundice include constitutional symptoms like malaise,
fatigue, and anorexia for a period of 1-2 weeks. In the acute phase, the typical clinical signs and
symptoms include nausea, vomiting, abdominal pain, and jaundice. In some cases, skin rashes,
joint pain, and arthritis may occur. Acute hepatitis B progresses to chronic HBV infection in 30-
90% of people infected as infants or young children and during adolescence or adulthood around
<5% of people infected may develop chronic infection. Chronic infection with HBV results in
chronic liver disease, including liver cirrhosis and hepatocellular carcinoma. In most of the cases,
the onset of hepatitis C infection is unrecognized because the clinical symptoms are often mild
and clinically not apparent. In symptomatic cases, clinical features include malaise, nausea,
vomiting, abdominal discomfort, pale stools, dark urine, and jaundice. Between 70% and 80%
develop chronic infections. Chronic infection is defined as infection persisting for more than 6
months with some evidence of hepatitis. The term chronic relates to the duration of infection and
not to the severity of the disease. Chronic hepatitis C infection leads to a wide spectrum of liver
diseases, ranging from mild hepatitis to cirrhosis, liver cancer and finally to liver failure in 10%
of the infected individuals.

Hepatitis B and C in oral cavity

HBV infection is the most important infectious occupational hazard in the dental
profession. Vectors of infection with HBV in dental practice include blood, saliva, and
nasopharyngeal secretions. Intraorally, the greatest concentration of hepatitis B infection is the
gingival sulcus. In addition, periodontal disease, severity of bleeding, and bad oral hygiene were
associated with the risk of HBV. In Egypt, patients with periodontal disease showed a higher
detectability rate of HBsAg, anti HBc, anti HCV, or both anti HCV and/or anti HBc in whole
unstimulated saliva than in the controls. HCV RNA has been detected in saliva and in salivary
glands from patients with sialadenitis. Most HCV patients (77%) had higher HCV RNA levels in
their gingival sulcus than in their saliva.

Oral manifestations of hepatitis B and C infection

Manifestations in the oral cavity include lichen planus, Sjögrens syndrome, and
sialadenitis, some forms of oral cancers may also be seen. Furthermore, cirrhotic patients may
have thrombocytopenia due to hypersplenism or treatment with interferon. In patients with liver
disease, the resultant impaired hemostasis can be manifested in the mouth as petechiaes or
excessive gingival bleeding with minor trauma. This is especially suggestive if it occurs in the
absence of inflammation. Therefore, special care must be taken during any type of surgery, oral
or otherwise; severe hemorrhage can ensue as a result of the paucity of clotting factors. An
interesting correlation exists between the increased prevalence of diabetes in patients with
chronic liver disease due to the severity of liver disease or to the treatment with interferon. HCV
may act as an independent diabetogenic factor. For the dentist this association has important
implications because diabetes is associated with significant changes in the oral cavity such as
increased frequency of periodontal disease, stomatitis, candidiasis, cheilitis, oral leukoplakia, and
dental caries.
Oral lichen planus and hepatitis
Lichen planus is a mucocutaneous disease of uncertain cause that affects the oral mucosa.
It is well documented that the disease represents a cell mediated immune response. Its prevalence
in the general population ranges from 0.1% to 2.2%, and the diagnostic criteria for OLP are
based on clinical and histopathologic features of the condition. It is classified as reticular, plaque,
atrophic, erosive, or bullous according to the clinical presentation. Emotional stress,
immunological disturbances, neurological dysfunctions, and viruses are possible etiological
factors. The prevalence of OLP and pitted keratolysis in the HBs Ag carrier group has been
found to be significantly high. HBs Ag positivity may induce or cause proneness to OLP and
pitted keratolysis with some mechanism that needs to be elucidated. Many studies and reports
suggest a positive correlation between the prevalence of hepatitis C and OLP, but some of them
still remain controversial. A recent case report suggests a correlation between the drugs and
interferons used for the treatment of hepatitis C with the extrahepatic manifestation such as OLP.
Some authors suggest that patients with HCV should undergo periodic oral examinations and
patients with OLP should undergo screening tests for HCV infection. The epidemiological
relationship between OLP and hepatitis C has been reported notably in the erosive type and
asymmetric lesions on the buccal mucosa. It has been seen that the prevalence of OLP associated
with hepatitis C presents geographical variations. Genetic variations among the populations seem
to be the main factor accounting for these differences. It is believed that HCV acts locally,
altering the function of the epithelial cells, or that the immune response of the host to HCV is
responsible for the development of OLP. Thus, host factors rather than geographic factors may
be more important in the pathogenesis of HCV related OLP.

Salivary gland disorders and hepatitis

The main salivary gland disorders associated with HCV infection are xerostomia,
Sjögren’s syndrome, and sialadenitis. Xerostomia increases patient vulnerability to caries and
oral soft tissue disorders, which, in combination with deficient hygiene, in turn facilitate the
development of candidiasis. It has not yet been demonstrated whether HCV infection causes
disease similar to primary Sjögren’s syndrome or whether it is directly responsible for the
development of Sjögren’s syndrome in certain types of patients. However, notoriously some
subjects can present a triple association of HCV infection, Sjögren’s syndrome, and sialadenitis
or salivary gland lymphoma. Although bacteria are the main cause of sialadenitis, viruses such as
HCV have been implicated as causes of sialadenitis associated with xerostomia. The role of
saliva includes cleaning, lubrication, chemical protection, and cell mediated and antibody
mediated immunity. Decrease in salivary flow may lead to dry mouth (particularly at night),
halitosis, dental decay, and difficulty in talking, eating, and swallowing. To make the patient
comfortable, one must take measures to effectively manage such cases. The patient should be
asked to take frequent sips of water or sugar free candies, which act as sialogogues and help
increase salivary flow. Prophylactic care including application of fluorides to prevent dental
decay must be taken. Patients may be advised to avoid hot and spicy food and use non foaming
toothpaste to increase oral comfort. Dietary counseling must be provided to control the frequency
and amount of carbohydrate.
Management of patients with hepatitis B and C infection in dental office
The most important and frequent problems associated with hepatitis B and C in dental
settings include the risk of viral contagion on the part of the dental professionals and rest of
patients (cross infection), the risk of bleeding in patients with serious liver disease, and
alterations in the metabolism of certain drug substances that increases the risk of toxicity. It has
been found that HBV and HCV exist on various surfaces in the dental operatory even many days
after treating patients positive with hepatitis B and C. HCV can remain stable at room
temperature for over 5 days. Therefore, standard precautions, i.e., the use of barrier methods,
with correct sterilization and disinfection measures, must be followed. The conventional
sterilization techniques usually eliminate specific proteins and nucleic acids (HBV DNA and
HCV RNA) from dental instruments previously infected with HBV and HCV. In case there is an
accidental exposure, follow these steps:
1. Carefully wash the wound without rubbing, as this may inoculate the virus into deeper tissues,
for several minutes with soap and water, or using a disinfectant of established efficacy against
the virus (iodine solutions or chlorine formulations). Some authors suggest that pressure should
be applied beneath the level of the wound to induce bleeding and thus help evacuate any possible
infectious material. However, no such fact has been strongly validated. The rationale behind
these measures is to reduce the number of viral units to below the threshold count required to
cause infection (the infectious dose). In this sense, dilution with water may lower the viral count
to below this threshold.
2. A complete detailed medical and clinical history of the patient must be recorded to rule out
possible risks.
Diagnosis of the disease
The disease can be diagnosed by quantifying the levels of HBV DNA, HBs Ag, and the
antigen/antibody ratio by means of immune enzymatic assays. Different enzyme linked
immunosorbent assay and recombinant immunoblot assay techniques have been developed for
the diagnosis, though the diagnostic gold standard remains detection of the viral genome using
real time polymerase chain reaction (RT PCR) technology. When the disease has developed and
the infection is well established, a liver biopsy must be performed to establish the amount of
fibrosis and the severity of the inflammation. These findings help the hepatologist determine the
treatment needs of the patients and help establish wise treatment decisions.

Management of exposures to hepatitis B virus

Any blood or body fluid exposure to an unvaccinated person should lead to the initiation
of the hepatitis B vaccine series (Recombivax HB® 10 mcg or Energix B® 20 mcg IM at 0, 1,
and 6 months). When hepatitis B Immune Globulin (HBIG) is indicated, it should be
administered as soon as possible after the exposure (preferable within 24 h, but it is
recommended up to 1 week following an occupational exposure). Hepatitis B vaccine can be
administered simultaneously with HBIG but at a separate site. Test for anti HBs must be
performed 1-2 months after the last dose of vaccine. Anti HBs cannot be ascertained if HBIG has
been administered within the previous 6 weeks.
Management of exposures to hepatitis C virus
On exposure to HCV, test for anti HCV must be carried out for the source. Baseline
testing for anti HCV and Alanine aminotransferase activity (ALT) should be carried out for the
exposed person. The most recent assays are based on the use of RT PCR). They can detect
minute amounts of HCV RNA (down to 10 international units (IU)/ml) and accurately quantify
HCV RNA levels up to approximately 107 IU/ml. Follow up testing for anti HCV and ALT
activity and HCV RNA by PCR at 4-6 weeks must be carried out for early detection. Results
reported positive by enzyme immunoassay with supplement test (e.g., Recombinant
immunoassay or HCV RNA by PCR) should be confirmed.
Before treating a patient infected with hepatitis B or C, a compilation of a detailed
clinical history is essential before dental treatment to identify patients posing possible risks,
together with a thorough oral examination. Consultation with the patient’s physician or specialist
is advisable to establish a safe and adequate treatment plan adapted to the medical condition of
the patient, considering the degree of liver functional impairment involved. Examination of the
oral cavity should assess any signs alerting to the existence of systemic disease. The patient
should receive an explanation of the risks associated with treatment, and informed consent is to
be obtained. In subjects with chronic hepatitis, it is important to determine the possible existence
of associated disorders (autoimmune processes, diabetes, etc.) to prevent their direct
complications and problems derived from specific medication use (corticosteroids and/or
immune suppressors). Liver disease may often be associated with a decrease in plasma
coagulation factor concentrations. In case any invasive procedure is to be performed in these
patients, prior coagulation and hemostasis tests are required, which include complete blood
count, bleeding time, prothrombin time/international normalized ratio (INR), thrombin time,
thromboplastin time, and liver biochemistry tests and the hematologist and hepatologist must
also be consulted.
Usually in an unfavorable state elective treatment is postponed; however, incase
treatment is carried out, the dentist must stock up on local hemostatic agents such as oxidized
and regenerated cellulose, as well as antifibrinolytic agents (tranexamic acid), fresh plasma,
platelets, and vitamin K. In some cases antibiotic prophylaxis is suggested, since liver
dysfunction is associated with diminished immune competence. Liver disease may result in
alterations in the metabolism of certain drugs. The physician treating the patient therefore should
be consulted to establish which drugs are used, their doses, and their possible interactions. The
administration of certain analgesics, antibiotics, and local anesthetics is generally well tolerated
by patients with mild to moderate liver dysfunction, though modifications might be necessary in
individuals with advanced stage liver disease. In this context, drugs metabolized in the liver may
have to be used with caution or their doses reduced and certain substances such as erythromycin,
metronidazole, or tetracyclines must be avoided entirely. Most of the antibiotics prescribed for
oral and maxillofacial infection scan be used in patients with chronic liver disease, and in general
the beta lactams can be administered. Aminoglycosides can increase the risk of liver toxicity in
patients with liver disease, and hence should be avoided. Nonsteroidal antiinflammatory drugs
should be used with caution or avoided, due to the risk of gastrointestinal bleeding and gastritis
usually associated with liver disease. Prophylaxis can be provided in the form of antacids or
histamine receptor antagonists. Local anesthetics are generally safe, provided the total dosage
does not exceed 7 mg/kg, combined with epinephrine.