Hepatitis

Know Thy Hepatitis: A Through TT

Several viruses have been identified as causative agents of hepatitis in humans. Other hepatotropic viruses have been implicated as potentially disease-causing. This article reviews the present knowledge of hepatitis A virus through the newly discovered hepatitis TT virus and their implication for dentistry.

Recent epidemiological data suggest that more than one in every 50 dental patients in the United States can be expect to be a chronic carrier of hepatitis B virus (HBV) or hepatitis C virus (HCV). Both of these viruses are associated with a high degree of morbidity and mortality. Other bloodborne and enterically transmitted hepatotropic viruses may also cause disease in humans, and it is important for oral health care providers to recognize the impact these viral infections have on dental practice standards. This article will provide an overview of hepatitis A through TT viruses and their implications in a dental setting.

The term "hepatitis" describes an inflammation of the liver but does not necessarily denote a cause or outcome of this specific condition. Although hepatitis as a disease has been recognized for more than 2,500 years, it was not until 1979 that the first "hepatitis virus" was isolated in cell culture.¹ Numerous toxic substances and pathogens, including several viruses, have been implicated in inducing hepatitis. From the 1940s through the 1960s, only an enterically transmitted infectious hepatitis virus and a parenterally transmitted serum hepatitis virus were recognized. These two viruses were designated hepatitis A virus (HAV) and hepatitis B virus, respectively. However, in 1965, Blumberg and colleagues identified the "Australian antigen," which was later shown to be part of the envelope protein of HBV.² With the ability to test for HBV in serum, it became clear that at least one more hepatitis-causing virus was present in blood. The existence of a third agent became even more evident in 1973 when specific tests could distinguish between HAV and HBV. This new transfusion-associated virus was coined non-A, non-B (NANB) as a new specific virus had not yet been identified, and a diagnosis was made by exclusion of HAV and HBV.³,⁴ Today, five distinct viruses causing disease in humans have been designated as hepatitis viruses. They are HAV, HBV, HCV, hepatitis D virus (HDV), and hepatitis E virus (HEV) (Table 1). HAV and HEV are mainly enterically transmitted while HBV, HCV, and HDV are most commonly transmitted parenterally. Although all these viruses share a common target organ, the liver, and may cause similar clinical signs and symptoms, they have very little else in common.

An additional two viruses, hepatitis G virus (HGV) and a virtually identical virus, hepatitis GB virus type C (GBV-C), have been discovered. But, unlike hepatitis A through E, no causal relationship has been established between HGV and GBV-C and acute hepatitis.⁵,⁶ Most recently, novel virus, designated as TTV, or TT virus, was discovered in 1997 and may be associated with post-transfusion hepatitis.⁷ A few cases of a hepatitis F virus (HFV) have been described in France, but it has not been linked to either acute or chronic disease in humans.⁸

Acute hepatitis in the United States is most commonly associated with HAV (47 percent), HBV (34 percent), or HCV (17 percent).⁹ Although acute hepatitis is associated with low morbidity, chronic hepatitis is linked to 16,000 deaths per year. Seventy percent of these cases are associated with HCV, 20 percent with HBV, and ¹⁰ percent with concomitant HCV and HBV infection.10 The rate of progression to permanent liver damage differs among types of viruses, yet cirrhosis and hepatocellular carcinoma (HCC) invariably follow long-term chronic infection. In cases of both HBV and HCV infections, it may take 25 to 30 years for HCC to develop. With co-infection of more than one virus, underlying chronic liver disease from other causes, or concomitant alcohol consumption, a much more rapid progression can occur.

Hepatitis A Virus

Hepatitis A virus is a single-stranded RNA virus belonging to the picornavirus family. Only one serotype of HAV has been recognized, and immunity to any of the seven known genotypes confers immunity and protection against all others.¹¹ Transmission of HAV occurs almost exclusively by the oral-fecal route. Primarily from person to person, but also by contaminated food or water. Transmission by blood can occur during the incubation period and the early acute phase, when titers as high as 105 infectious doses per milliliter of blood have been documented.¹² Although rare, transmission of HAV by blood transfusion has been reported.¹³ Even though HAV can be detected in saliva during the incubation period, transmission by saliva has not been reported.¹⁴ Most exposures to HAV, as with most exposures to all hepatitis viruses, are from unknown sources.

The incubation period of HAV infection ranges from 15 to 50 days with an average of 28 days. However, the two weeks preceding clinical signs of the disease are considered the most infectious period. Immunoglobulin M (IgM) anti-HAV can be detected in the serum five days following exposure to HAV while IgG anti-HAV is produced during the convalescent phase. This latter immunoglobulin will confer lifelong protection against reinfection.

Hepatitis A is an acute, self-limiting disease with symptoms typically lasting for approximately two weeks, but they may persist for as long as two to six months.¹⁵ Prognosis for patients contracting HAV infection is good, and a chronic state does not develop. The severity of HAV infection increases with age and in individuals with underlying chronic liver disease from other causes. It is estimated that the mortality rate of hepatitis A infection in the United States is less than 0.2 percent, which results in approximately 100 deaths per year. In children younger than 6, 70 percent of infections are asymptomatic, while more than 70 percent of infections in older children and adults are symptomatic.

There are two hepatitis A vaccines licensed in the United States, Havrix (SmithKline Beecham Pharmaceuticals) and Vaqta (Merck & Co., Inc.). Both vaccines contain formalin-inactivated viral particles and are equally effective in conferring up to 100 percent protection against symptomatic hepatitis A.¹⁶,¹⁷

There is also a combination hepatitis A and B vaccine, Twinrix (SmithKline Beecham Pharmaceuticals), that may be used for travelers to endemic areas.¹⁸

Hepatitis A is not considered an occupational hazard to dentists, and routine vaccination for dental personnel is not recommended.

Hepatitis E Virus

Hepatitis E virus, a single-stranded RNA virus closely resembling the calicivirus family, was first described in 1983.¹⁹ As with HAV, HEV is an enterically transmitted virus, mainly through fecally contaminated water. Interestingly, even though anti-HEV may be found in 1 percent to 5 percent of blood donors in the United States,²⁰ this virus rarely causes disease in this country. However, HEV poses a risk to people traveling to endemic regions.²¹ Signs and symptoms of HEV disease are similar to those of HAV, and it has an incubation period averaging 40 days. During the incubation period, viremia is present; but an infectious titer has not been determined. An increased mortality rate, of up to 30 percent, has been reported among pregnant women outside the United States.²² Protective immunity after exposure has not been documented, and no human vaccine is available.²³

Similarly to HAV, HEV is not associated with a chronic disease state and poses no occupational risk to dental providers.

Hepatitis B Virus

Evidence of the hepatitis B virus was first reported in 1965,2 and it was soon evident that this virus was a leading cause of chronic hepatitis, cirrhosis, and primary HCC. It is estimated that more than 350 million people are infected worldwide, with 1.25 million chronic HBV carriers in the United States.²⁴ The most common modes of transmission in the United States are sexual contact and injection drug use. However, occupational exposure in health care settings also occurs. Other, much less common, modes of transmission include that of infected health care workers to patients.²⁵ Nine clusters of infected patients have been documented where dentists have been identified as the source of HBV.²⁶ However, no HBV transmission from a dentist has been documented since 1987. Large quantities of HBV can be found in serum of infected individuals, 108 to 1010 virions/ml, but also to a lesser extent in other body fluids, including saliva, making this virus highly infectious. It is estimated that the risk of acquiring HBV infection after a percutaneous needlestick from an HBeAg carrier is approximately 30 percent, while the risk decreases to approximately 6 percent if the carrier is only a hepatitis B surface antigen-positive carrier.²⁷ Dentists are at an increased risk of acquiring HBV compared to the general population, but this risk is drastically reduced by employing standard precautions, including immunizations.²⁸

Hepatitis B is a double-stranded DNA virus belonging to the hepadnavirus family. Five genotypes of HBV have been reported, all of the same serotype. The incubation period for HBV infection ranges from 45 to 160 days, and the ensuing disease is associated with a mortality rate of 0.2 percent to 2.0 percent. The immune response to HBV is complex but determines the outcome of the infection, both the hepatic damage and protective immunity. Among healthy adults, the infection is self-limiting in 95 percent of cases resulting in the production of protective antibodies indicating resolution, while 3 percent to 5 percent remain chronically infected.²⁹ The opposite is found among infected infants; 95 percent become chronic carriers.

There are several serological markers associated with HBV infection that will indicate the status of the disease (Table 2). The whole virion, also called the Dane particle, is a sphere containing a core that encloses the viral DNA. The outside envelope is associated with the hepatitis B surface antigen, or HBsAg. Development of cellular and specifically humoral immunity to HBsAg, anti-HBsAg, will confer protection from reinfection. The production of these antibodies is also the basis for the two HBV vaccines available in the United States. The antigen associated with the viral core, the hepatitis B core antigen, or HBcAg, induces the cellular immune response that is ultimately responsible for destroying cells infected with HBV. Routine serologic assessment of HBcAg is not available, but anti-HBcAg is used to determine exposure to HBV because it is present in all people exposed to HBV. This antibody, unlike anti-HBsAg, is not protective but instead is used to distinguish acute from chronic infections. The early antibody to HBcAg, IgM-HBcAg, usually disappears within a couple of months of an acute infection but can sometimes resurface during flare-ups in chronic HBV carriers.

Another antigen derived from the core gene, hepatitis B e antigen, or HBeAg, is a marker for active viral replication. Although HBeAg-positive individuals are regarded as highly infectious, there is a group of infected individuals with a precore mutant strain of HBV that prevents expression of HBeAg, yet allows for expression of infectious virus.³⁰ A more accurate expression of viral replication and infectivity is the presence of HBV DNA in serum. There are no standardized tests to determine the degree of infectivity of an individual based on quantitative HBV DNA analysis or level of HBeAg. Furthermore, detection of HBV DNA in both in serum and peripheral blood mononuclear cells after a serological cure suggests that reactivation of infection may occur due to immune suppression.³¹

The vigor of the infected person's immune response will determine the outcome of the infection. If the immune response is successful, there is complete destruction of all infected cells, halted viral replication, and production of protective antibodies. If the immune response is inadequate, or if the infected person's immune system does not have the means to eradicate the infection, a chronic state will ensue.³² Hepatitis B is not cytopathic in itself; instead, it is the persistent immune assault in chronically infected individuals that is ultimately responsible for liver complications. The constant inflammatory state and repeated cellular generation increases the risk for the development of cirrhosis and HCC. It is estimated that chronic carriers of HBsAg have a 12- to 79-fold increased risk of dying from cirrhosis as compared to healthy individuals.³³

A plasma-derived vaccine, Heptavax-B (Merck & Co., Inc.) was introduced in the United States in 1981; and later two recombinant vaccines, Recombivax HB (Merck & Co., Inc.) in 1987 and Engerix-B (SmithKline Beecham Pharmaceuticals) in 1989, were licensed and are now available. These vaccines have proven to be highly effective, protecting more than 96 percent of vaccinated young, healthy adults. The acceptance of these vaccines has resulted in a decline from 17,000 annual HBV infections among health care workers in 1983 to only 400 in 1995.³⁴ In 1983, the incidence of HBV infections among health care workers was 386 per 100,000 but has since declined dramatically to 9.1 per 100,000 in 1995, which is less than one-fifth the incidence of HBV among the general population (50 per 100,000). Investigations of the long-term (five-to-11-year), effect of HBV vaccination have revealed no acute or chronic cases of HBV among vaccine responders, although 2.6 percent developed anti-HBeAg, suggesting subclinical infections.34 These longitudinal investigations indicate that vaccine-induced protection from HBV persists for at least 11 years. Although guidelines have suggested that individuals with antibody levels below 10 mIU should receive booster doses, this has not been substantiated in clinical studies. Subsequently, recommendations have been proposed to limit booster doses only to individuals who have demonstrated failure of the vaccine to protect against clinically significant HBV infection, viremia, or development of chronic infection.34

Hepatitis D Virus

Hepatitis D virus was initially reported by Rizzetto and colleagues in 1977 as a co-infection with HBV.³⁵ This defective negative-stranded RNA virus is unique among animal viruses because it depends on HBV for propagation. Although transmissibility is dependent on the HBsAg, HDV virions can replicate without the helper HBV.³⁶ The HBV virion consists of the HDV RNA genome, a hepatitis delta antigen (HDAg), and an envelope of HBsAg. Thus, the infectivity and survival of HDV depends on the integrity of HBV since HDV needs only the HBsAg to form the envelope of the virus. Once the HDV virion or genome is within a permissive cell, it can replicate without the helper HBV.

There are three different HDV genotypes with different geographic and demographic distributions and, possibly, severity of disease.³⁷ Genotype 1 is the predominant type in North America and Europe. In the United States, HDV infections are most commonly found among injecting drug users and hemophiliacs.³⁸ The incubation period for HDV averages 35 days and carries a mortality rate of from 2 percent up to 20 percent.³⁹

Co-infection of HBV and HDV implies a simultaneous exposure to the two viruses, while superinfection consists of HDV exposure of an already chronic carrier of HBV. Acute co-infections are mostly self-limiting with approximately 2 percent to 5 percent of exposed individuals becoming chronic carriers of both viruses. Superinfections are commonly not resolved spontaneously, with 70 percent to 80 percent of infected individuals becoming chronic carriers. Chronic HDV infections often progress to cirrhosis, accounting for approximately 50 percent of this condition among chronic HBsAg carriers.⁴⁰

Immunization with HBV vaccine also confers immunity to HDV.

Hepatitis C Virus

It is estimated that 3.9 million Americans, or 1.8 percent, are chronically infected with the hepatitis C virus, making HCV infection the most common bloodborne infection in the United States.⁴¹ However, this may be a conservative estimate because many individuals at high risk for HCV are not included in the national surveys conducted to establish prevalence of infections such as HCV.

HCV is an RNA virus with at least six different genotypes and more than 90 subtypes.⁴² The most common genotype in the United States is type 1, which accounts for approximately 70 percent of infections.⁴³ The virus mutates often, and an infected individual may carry a heterogeneous population of HCV and even different types. It is possible that this genetic diversity enables the virus to escape the body's immune surveillance, causing its high chronicity rate.

The rate of new infections has declined dramatically since the cloning of the virus in 1988, from an average of 230,000 to 36,000 infections per year by 1996.⁴⁴ However, due to the high rate of chronicity (85 percent to 90 percent of all individuals infected with HCV) and poor long-term response to therapy, deaths related to chronic HCV are expected to increase dramatically. It is estimated that 20 percent of all individuals assessed in inner-city emergency rooms and more than 30 percent of prison inmates are carriers of HCV.

Infected individuals develop antibodies to HCV that can be detected serologically. These antibodies are markers of infection but do not confer immunity, and only 10 percent to 15 percent of acutely infected individuals have a self-limited disease.

Only 25 percent to 35 percent of individuals with acute HCV infections will exhibit clinical symptoms, such as malaise, anorexia and jaundice, which may appear on an average of six to seven weeks after exposure. This low rate of clinical disease contributes to the high incidence of infected individuals not being aware of their infectious status. The major causes of death secondary to chronic HCV infection are cirrhosis, liver failure, and HCC. Over a period of 20 to 30 years, 10 percent to 20 percent of chronically infected individuals will develop cirrhosis, while 1 percent to 5 percent develop HCC. A combination of cirrhosis and HCC may result in a rate of HCC as high as 1 percent to 4 percent per year. It appears that geographic variations, age greater than 40 at the time of acquiring the infection, male gender, co-infection with other viruses such as HIV and HSV, and alcohol consumption are all associated with increased severity of disease. Mode of transmission may be a risk factor to develop complications secondary to HCV infection. Patients with post-transfusion HCV appear to be at a greater risk to develop progressive liver complications, particularly hepatic cirrhosis, compared to people contracting HCV through other modes of transmission.⁴⁵ Serum albumin, prothrombin time, and platelet count are independent laboratory predictors of progressive hepatic destruction.45 The effect of alcohol consumption on HCV infection has been debated. It appears that total lifetime alcohol consumption as well as even very low levels of continuous alcohol consumption by HCV carriers will have a detrimental effect on disease outcome, increasing viremia and hepatic cirrhosis.⁴⁶,⁴⁷

Presently, the annual mortality rate of HCV in the United States is more than 10,000, but this number is expected to triple in the next 20 to 30 years.

Extrahepatic manifestations of HCV have been reported. Two of these conditions are of interest to dentists -- lichen planus and a Sjögren-like syndrome. Several studies have suggested that individuals with lichen planus have a high prevalence, 34 percent to 62 percent, of HCV.⁴⁸,⁴⁹ Furthermore, patients with chronic HCV infections have been found to have a higher prevalence of lichen planus compared with the general population.⁵⁰,⁵¹ Most of these studies have been performed in Italy and Japan, whereas epidemiological studies from the United States have yet to show a significant association between lichen planus and HCV. It has been suggested that such a relationship may have a geographic predilection.

A Sjögren-like syndrome has also been associated with HCV-infection.36 It has been documented that HCV-infected individuals have both salivary and lacrimal abnormalities, and it has also been reported that up to 40 percent of individuals with Sjögren's syndrome may have HCV infections.⁵² A relationship between virus infections and salivary gland dysfunction has been reported with other viruses and although the exact pathogenesis of this association has not been elucidated, it is possible that HCV may exert a similar effect.

Another confounding relationship has been suggested between HCV and oral cancer. Studies from Japan have indicated a high prevalence of HCV infection among patients with oral cancer.⁵³ It is not clear if HCV has a causative relationship with the development of oral neoplasms or if the presence of the infection is only an indicator.

Treatment of HCV infection with interferon has not shown long-term efficacy and seems to be a function of its genotype. HCV type 1 is associated with more progressive liver disease and poor response to interferon treatment.43 Combination therapy with interferon and ribavirin may have a beneficial effect on disease progression. Recent studies have indicated that initial treatment, as well as treatment of patients after relapse of chronic HCV infection, with interferon and ribavirin may produce a sustained undetectable viral load.⁵⁴ In the initial treatment group, 38 percent of patients showed undetectable serum HCV RNA after 48 weeks, while 49 percent of patients in the relapse group had undetectable serum HCV RNA after 24 weeks.

HCV is mainly transmitted by direct percutaneous exposure to contaminated blood, primarily through blood transfusions and by injection drug use.⁴⁴ However, since the institution of effective screening processes for HCV in donated blood in May 1990 and again in July of 1992, no transfusion-associated HCV infection has been reported to the Centers for Disease Control and Prevention. Still, it is estimated that the risk of acquiring HCV through blood transfusions in the United States is 0.001 percent per unit transfused. The highest prevalence of HCV is found among injection drug users, which accounts for approximately 60 percent of all new infections⁴⁴ (Table 3). The risk of sexual transmission of HCV is slight, yet contributes to a high number of HCV infections. It is estimated that 1 percent of sexual partners of HCV-infected individuals will be infected per year.⁵⁵ This risk can be reduced to one-sixth of that figure by giving uninfected partners bimonthly injections with immune serum globulin.55 As with many other bloodborne viral infections, the risk of transmission is higher from male to female than from female to male.

Only tests measuring anti-HCV are approved by the U.S. Food and Drug Administration for diagnosis of HCV infection. The sensitivity of these tests is more than 97 percent, but they cannot discriminate between acute, chronic, or resolved stages of infection.⁵⁶ The average time between exposure and seroconversion is estimated to be from eight to nine weeks. Within 15 weeks after exposure, 80 percent of infected individuals will demonstrate presence of anti-HCV, while more than 90 percent of infected individuals will have detectable anti-HCV within five months after exposure. A diagnosis of HCV infection can also be established by qualitative measurements of HCV RNA by polymerase chain reaction. HCV RNA can be detected one to two weeks after exposure, which is before the appearance of both abnormal liver function tests, such as alanine aminotransferase, and anti-HCV.

HCV transmission from patients to health care workers has been documented.⁵⁷ The seroconversion rate after a percutaneous injury varies from 0 percent to 7 percent but may be higher, possibly dependent on geographical variations and infectivity of the patient.⁵⁸,⁵⁹ There are no standardized assays to determine infectivity. Furthermore, it is not known what concentration of HCV is necessary to establish infection.

HCV RNA has been detected on surfaces in a dental operatory after treatment of an HCV-infected patient.⁶⁰ Although HCV RNA can be detected on surfaces in room temperature for up to five days, it is not clear if inert contaminated objects can transmit HCV. HCV RNA can also be found in saliva from HCV-positive individuals, and it has been suggested that transmission of HCV has occurred through human bites.⁶¹,⁶² Although dentists are exposed to both saliva and blood, epidemiological studies have not indicated that dentists are at an increased occupational risk of contracting HCV.28 In cases of percutaneous injuries, no prophylaxis is recommended because no postexposure measures have shown to be effective.⁶³ It appears that for interferon to have a beneficial response, an established infection need to be present.

Hepatitis G Virus

In 1995, two independent groups of researchers identified a new agent tentatively called GB virus C (GBV-C) or hepatitis G virus (HGV).⁶⁴,⁶⁵ GBV-C was discovered in a 34-year-old surgeon, with the initials GB, who presented with acute sporadic hepatitis, while HGV was isolated from a HCV carrier. Subsequently it was shown that these two agents represented the same virus with a homology of 86 percent and 95 percent of its nucleotide level and amino acid level, respectively.⁶⁶ Three, and possibly four, major groups of HGV have been identified in various regions of the world.⁶⁷ It is not clear if different variants are the reason for the difference in prevalence seen in geographically separate areas. Studies have indicated prevalence rates of up to 15 percent in West Africa to less than 1 percent to 2 percent in the United States.⁶⁸ Much higher prevalence rates have been documented in the United States in subsets of patient populations such as intravenous drug users (15.8 percent to 33.3 percent).68 A higher prevalence can also be expected among hemodialysis patients and hemophiliacs. It is clear that the primary mode of transmission of HGV is parenteral as in multiple blood transfusions. Vertical and sexual transmissions have been documented; but other modes of transmission may also be present since HGV has been found in numerous body fluids, including saliva.⁶⁹ Nonparenteral transmission of HGV may also occur as suggested by the high proportion of HGV seen in apparently healthy blood donors and in the general population.⁷⁰

The question that needs to be answered is if HGV actually causes disease. There is little evidence that HGV independently can cause hepatitis, since the vast majority of patients with HGV and hepatitis are also infected with either HBV and/or HCV. Also, the high prevalence of HGV viremia in the general population without any indication of hepatitis would further support the assumption that HGV is not independently responsible for causing disease. However, it has been speculated that although HGV seems to be benign in most cases, it may become virulent under certain conditions.70

TT Virus

The latest of hepatitis viruses has been named TT virus, or TTV.7 "TT" are the initials of the Japanese patients from whom the virus was isolated and cloned. However, "TT" is also used to designate this virus as the "transfusion-transmitted" virus.⁷¹ The prevalence of TTV among patients with liver disease is not known, but TTV DNA has been detected in 25 percent of 72 patients with chronic liver disease and in 10 percent of individuals without liver disease.⁷¹ Reports from North America suggest a prevalence of TTV of 1 percent among blood donors, 15 percent among patients with cryptogenic cirrhosis, 27 percent among patients with fulminant hepatic failure, 18 percent among individuals exposed to blood products, and 4 percent among individuals without parenteral risk factors.⁷²

It is not yet clear if this virus, similar to HGV, is a disease-causing agent in humans, although there are suggestions that TTV may be responsible for non-A-G post-transfusion hepatitis.⁷³

Dental Considerations

The main concerns for oral health care providers treating chronic HBV and HCV carriers are contagion and liver abnormalities. Employment of standard precautions, including appropriate immunization, has shown to decrease occupational transmission of both HBV and HCV. Although total elimination of risk cannot be achieved and personal bias as to what constitutes a risk always needs to be considered, the occupational hazard to oral health care providers who are using standard precautions are at a professionally acceptable level. It is estimated that dentists sustain an average of approximately two percutaneous injuries per year. Such injuries are obviously accompanied by a risk of exposure to bloodborne pathogens. Therefore, after percutaneous exposures, it is advisable to obtain permission from the source patient to have his or her blood tested for anti-HCV; HBsAg, when the health care worker is not immune to HBV; and human immunodeficiency virus. Post-exposure prophylaxis is not advisable for exposure to HCV; but for health care workers susceptible to HBV, specific guidelines have been proposed (Table 4). Postexposure prophylaxis guidelines for HIV have also been published.⁷⁵

The vast majority of chronic hepatitis HBV and HCV patients are asymptomatic and unaware of their infectious status. There is no need to modify any dental practices for these patients. Any patient identified as high risk for acquiring either HBV or HCV should be encouraged to be tested because early recognition of disease will decrease morbidity as well as subsequent transmissions.

Patients exhibiting liver disease secondary to their viral infection need to be assessed for extent of liver damage. Up to 80 percent of the liver can be destroyed before impaired hemostasis and drug metabolism become evident. Both of these conditions have an important impact on provision of dental care. Although elevated liver transaminases indicate active liver cell damage, liver function can be assessed for the purpose of dental care by a prothrombin time test.⁷⁶ Any general dental procedures, including simple extractions, can be safely performed in patients with a normal prothrombin time (10 to 12 seconds) and a platelet count above 60,000 per milliliter. Administration of lidocaine for local anesthesia for dental procedures can be utilized in patients with moderate to severe liver disease. However, certain analgesics, such as acetaminophen, need to be used with caution.⁷⁶ Patients with liver disease are not usually more susceptible to infections, and routine antibiotic prophylaxis is not indicated.

Summary

The growing population of chronic hepatitis virus carriers poses a challenge to dental professionals. Increased understanding of the pathogenesis and transmission of these viruses will impact implementation of appropriate dental practices. Furthermore, incorporation of oral health care providers into the overall health care of patients will enhance the quality of life for infected individuals.

Author

Michael Glick, DMD, is the Director of Programs for Medically Complex Patients in the Department of Oral Medicine at the University of Pennsylvania School of Dental Medicine.

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