Viral hepatitis is an inflammation of the liver caused by infectious hepatitis viruses. There are 5 main hepatitis viruses - Hepatitis A, B, C, D, and E. Hepatitis A is transmitted through the fecal-oral route while Hepatitis B can be transmitted sexually or parenterally. Hepatitis C is commonly spread through intravenous drug use or blood transfusions. Hepatitis D only infects those also infected with Hepatitis B. Hepatitis E is also spread through the fecal-oral route. Acute viral hepatitis presents with fatigue, nausea, abdominal pain and jaundice while chronic hepatitis from some viruses can lead to cirrhosis or liver cancer over many years.

1. VIRAL HEPATITIS

3. CONTENTS
 Definition and Classification
 Physiology
 Pathogenesis
 Complications
 Individual Viruses
 Dental Considerations
 References

4. HISTORY
 Its an ancient disease first described in 5th century BC
 Earliest recognized blood-borne outbreak of hepatitis was
in Germany in 1883 after receiving small pox vaccine
 In 1947, McCalum and Bauer introduced the term hepatitis
A for infectious and Hepatitis B for serum hepatitis.
 This terminology was adopted by WHO in 1973

5. HEPATITIS
 DEFINITION: Hepatitis is inflammation of the liver that
may result from infectious or other causes.
 Examples of hepatitis with infectious causes are viral
hepatitis, infectious mononucleosis, secondary syphilis, and
tuberculosis,etc
 Noninfectious hepatitis can result from excessive or
prolonged use of toxic substances (e.g., drugs
[acetaminophen, alcohol, halothane, ketoconazole,
methyldopa, methotrexate]; more commonly,
alcohol),auto-immune

6.  Acute Hepatitis- is a self limited liver injury of less than 6
months.
 Chronic Hepatitis is defined as symptomatic, biochemical
or serologic evidence of continuing or relapsing hepatic
disease for more than 6 months with histologically
documented inflammation and necrosis.
 Fulminant hepatitis- when hepatic insufficiency progresses
from onset of symptoms to hepatic encephalopathy within
2-3 weeks

7. Diagnosis
 Liver function tests (AST and ALT elevated out of
proportion to alkaline phosphatase, usually with
hyperbilirubinemia)
 Viral serologic testing
 PT/INR measurement

8. Pathogenesis

10. PATHOPHYSIOLOGY AND COMPLICATIONS
 Hepatitis viruses replicate in hepatocytes and ultimately
damage the host cell.
 HBV infection produces high serum titers that may reach 10 8
to 10 11 virions/mL.
 In contrast, HAV produces a viremia that may reach 10 5
virions/mL in blood but 10 6 to 10 10 genomes/g in stool.
 No single histopathologic lesion is characteristic of viral
hepatitis, but the appearances of types A, B, C, D, and E
hepatitides are similar and are described together.
 Commonly, acute viral hepatitis is characterized by ballooning
degeneration and necrosis of liver cells (hepatocytes). The
entire liver lobule becomes inflamed and consists of
lymphocytes and mononuclear phagocytes.

11.  Icterus (jaundice) is associated with hepatitis in
 approximately 70% of cases of HAV,
 approximately 30% of cases of HBV infection, and
 approximately 25% of cases of HCV and HEV.
 This is caused by an accumulation of bilirubin in the
plasma, epithelium, and urine.

12.  Jaundice usually becomes clinically apparent when the plasma level of
bilirubin approaches 2.5 mg/100 mL (normal is less than 1 mg/100
mL).
 If plasma bilirubin does not reach this level, the patient is
anicteric(without jaundice), thus explaining nonicteric hepatitis.

13.  Most cases of viral hepatitis, especially types A and E, resolve with no
complications.
 HBV, HCV, and HDV may persist and can replicate in the liver when
the virus is not completely cleared from the organ.

14.  The consequences of hepatitis include
-recovery,
-persistent infection (or carrier state),
-dual infection, chronic active hepatitis,
-fulminant hepatitis,
-cirrhosis,
-hepatocellular carcinoma, and
-death.

15. CLINICAL PRESENTATION
 Patients classically exhibit three phases of acute illness.
 The prodromal (preicteric) phase,
which usually precedes the onset of jaundice by 1 or 2 weeks, consists of
— abdominal pain,
— anorexia,
— intermittent nausea,
— vomiting,
— fatigue,
— myalgia,
— malaise, and
— fever.
 With hepatitis B, 5% to 10% of patients demonstrate serum sickness–like
manifestations, including arthralgia or arthritis, rash, and angioedema.

16.  The icteric phase
 Onset of clinical jaundice,
 Many nonspecific prodromal symptoms may subside, but
gastrointestinal symptoms (e.g., anorexia, nausea, vomiting, right
upper quadrant pain) may increase, especially early in the phase.
 Hepatomegaly and splenomegaly frequently are seen.
 This phase lasts 2 to 8 weeks

17.  During the convalescent or recovery (posticteric) phase,
 symptoms disappear, but hepatomegaly and abnormal liver
function values may persist for a variable period.
 This phase can last for weeks or months, and recovery time for
hepatitis B and C is generally longer.
 HBV infrequently is associated with clinical syndromes, including
polyarteritis nodosa, glomerulonephritis, and leukocytoclastic
vasculitis.
 Coagulopathy, encephalopathy, cerebral edema, and fulminant
hepatitis are rare.
 Nonspecific symptoms of chronic hepatitis C (loss of weight, easy
fatigue, sleep disorder, difficulty in concentrating, right upper
quadrant pain, and liver tenderness) may not appear until hepatic
fibrosis, cirrhosis, or hepatocellular carcinoma is present.

18.  Hepatic damage is caused by the cytopathic effects of the virus and
inflammatory changes related to immune activation.
 Extrahepatic immunologic disorders associated with chronic HCV
infection result from the production of autoantibodies and include
immune complex–mediated disease (vasculitis, polyarteritis
nodosa),
autoimmune disorders (rheumatoid arthritis, glomerulonephritis,
thrombocytopenic purpura, thyroiditis, pulmonary fibrosis), and
two immunologic disorders: lichen planus and Sjögren's-like
syndrome (lymphocytic sialadenitis).
 If these diseases or signs of advanced liver disease (bleeding
esophageal varices, ascites, jaundice, spider angioma, dark urine)
are noted, testing for chronic hepatitis is recommended.

19.  HDV infection often results in severe acute hepatitis or
rapidly progressive chronic liver disease.
 Coinfection usually leads to transient and self-limiting
disease, whereas superinfection more often results in
severe clinical disease, indicated by sudden exacerbation in
a chronic carrier of HBV.

22. HEPATITIS A
 Caused by HAV, seen where socio-economic and living
conditions are poor
 Spread- mainly faeco-oral but can be transmitted sexually
 Incubation period- 2-6 weeks
 Subclinical disease
 Cl/f include fatigue, nausea and vomiting, abdominal pain,
loss of appetite, low grade fever, jaundice and itching.
 Recovery- uneventful
 No evidence of a carrier state or progression to CLD

24. HEPATITIS B
 Serum hepatitis, homologous serum jaundice
 It affects 1/3rd of the world’s population and 1/4th of those infected at
birth die from liver disease
 Endemic, common in developing world
 Australia Antigen
 Spread is mainly parenteral– via unscreened blood or blood products,
intravenous drug abuse, tattooing, sexual and perinatal.
 Incubation period is 2-6 months.
 About 30% have no signs and symptoms
 Effects range from subclinical infection to fulminating hepatitis, acute
hepatic failure and death.

25.  Prodrome period – 1-2 weeks- anorexia, malaise and nausea
 Hep B viremia usually precedes the clinical illness by weeks or months
 As jaundice becomes evident- stools become pale and urine dark due to
bilirubinuria.
 Liver –enlarged and tender, pruritis
 Muscle pains, rashes and arthalgia- more in Hep B than Hep A
 Complications include:
-Carrier state
-Chronic infection
-Cirrhosis
-HCC
-Polyarteritis nodosa
-Death

26. Acute viral hepatitis: biochemical features

27.  Carrier state, in which HBV persists within the body for > 6months
develops in 5-10% of people with chronic infection
 Immune tolerance
 Immune clearance
 Low replication
 Reactivation
 Frequent in anicteric infections or those contracted early in life
 High risk- received blood products, those infected with HDV, and
immune defects
 Most carriers- healthy, others with persistently abnormal LFTs develop
CLD and 15-25% die from it.

32. Hepacard test
 It is a visual rapid accurate one step immunoassay for
detection of HBsAg
 100% sensitivity and 98% specificity

33. HEPATITIS C
 Identified from post transfusion NANBH
 Spread- IV drug users, blood products, renal dialysis,etc
 6 major genotypes present
 Similar incubation to HBV and infection is usually less severe- but 25-
80% have abnormal LFTs > CLD
 <3% develop liver cancer, or die
 Present in saliva, 10% of needlestick injuries
 Passive and active immunoprophylaxis against HCV is mot present

35. HEPATITIS D
 HDV( delta agent) is a single-stranded RNA viroid (incomplete virus) –
replicative capacity of HBV to infect and replicate in humans
 Spread- parenterally
 Endemic – Mediterranean and among IV drug abusers
 Biphasic pattern
 90% of infections are asymptomatic but can cause fulminant disease
with high mortality
 About 70-80% HBV carriers with HDV superinfection progress to CLD
with cirrhosis > 15-30% with chronic HBV infection alone
 There is no effective HDV immunoprophylaxis

37. HEPATITIS E
 HEVis a single-stranded RNA virus belonging to the Calici virus family
 Spread- faeco-oral
 Unlike others, mortality rate in pregnant women is high(15-20%)
 HEV infections resolve spontaneously and do not progress to chronic
hepatitis
 Currently licensed hepatitis E vaccine - (HEV 239 vaccine,Hecolin)

38. HEPATITIS G
 Relatively new virus, previously thought of as HCV
 Diagnosed- HGV RNA in serum
 Transmission is mainly seen in the dialysis setting and also IV drug
users
 Co-infection possible with HBV or HCV
 Infection is less severe than HCV

39. GENERAL TREATMENT
 As with many viral diseases, basic therapy is palliative
and supportive.
 Bed rest and fluids may be prescribed, especially during
the acute phase.
 A nutritious, high-calorie diet is advised.
 Alcohol and drugs metabolized by the liver are not to be
ingested.
 Viral antigen and ALT levels should be monitored for 6
months
 Standard therapy for patients with chronic hepatitis is
interferon (IFN) alfa-2b (3 to 10 million units)
administered three times weekly for 6 months to 1 year.

40.  Newer modalities have used the pegylated form of IFN with
better sustained virologic response.
 IFN therapy normalizes ALT levels in up to 17% of patients
infected with HDV, 30% of those infected with HCV, and
40% of those infected with HBV and reduces the risk for
development of hepatocellular carcinoma.
 Adverse effects (e.g., fatigue, flulike symptoms, bone
marrow suppression) are common.

41.  The addition of lamivudine (a nucleoside analog active
against HBV) or ribavirin (a guanosine analog active
against HCV) results in a virologic response in an
additional 15% to 25%.
 Corticosteroids are usually reserved for fulminant hepatitis.
 Liver transplantation is a last resort for patients who
develop cirrhosis

42. ORAL MANIFESTATIONS
 The oral cavity can reflect liver dysfunction in the form of
mucosal membrane jaundice, bleeding disorders, petechiae,
increased vulnerability to bruising, gingivitis, gingival
bleeding (even in response to minimum trauma) ,foetor
hepaticus (a characteristic odor of advanced liver disease),
cheilitis, smooth and atrophic tongue, xerostomia, bruxism
and crusted perioral rash.In these patients, chronic
periodontal disease is a common finding

43. DENTAL MANAGEMENT
 Identification of potential or actual carriers of HBV, HCV, and
HDV is problematic because in most instances, carriers
cannot be identified by history.
 The inability to identify potentially infectious patients extends
to HIV infection and other sexually transmitted diseases.
 Therefore, all patients with a history of viral hepatitis must be
managed as though they are potentially infectious.
 Recommendations for infection control practices in dentistry
published by the CDC and the American Dental Association
have become the standard of care for preventing
crossinfection in dental practice .
 All dental health care workers who provide patient care
should receive vaccination against hepatitis B virus

44.  . The most frequent problems associated with liver disease
in clinical practice refer to
1. the risk of viral contagion on the part of the dental
professionals and rest of patients (cross-infection),
2. the risk of bleeding in patients with serious liver disease,
3. and alterations in the metabolism of certain drug
substances – which increases the risk of toxicity

45.  Patients With Active Hepatitis.
 No dental treatment other than urgent care (absolutely
necessary work) should be rendered unless the patient is
clinically and biochemically recovered.
 Urgent care should be provided only in an isolated
operatory with adherence to strict standard precautions.
 Aerosols should be minimized and drugs metabolized in the
liver should be avoided as much as possible.
 If surgery is necessary, preoperative prothrombin time and
bleeding time should be obtained and abnormal results
discussed with the physician.
 The dentist should refer the patient who has acute hepatitis
for medical diagnosis and treatment.

46.  Patients With a History of Hepatitis.
 Most carriers of HBV, HCV, and HDV are unaware that they
have had hepatitis.
 An additional consideration in patients with a history of
hepatitis of unknown type is the use of the clinical laboratory
to screen for the presence of HBsAg or anti-HCV.
 Patients at High Risk for HBV or HCV Infection.
 Several groups are at unusually high risk for HBV and HCV
infection.
 Screening for HBsAg and anti-HCV is recommended for
individuals who fit into one or more of these categories unless
they are already known to be seropositive.
 In addition, the patient might have undetected chronic active
hepatitis, which could lead to bleeding complications or drug
metabolism problems.

47.  Patients Who Are Hepatitis Carriers.
 In addition, some hepatitis carriers may have chronic active
hepatitis, leading to compromised liver function and
interference with hemostasis and drug metabolism.
 Physician consultation and laboratory screening of liver
function are advised for determination of current status and
future risks.
 Patients With Signs or Symptoms of Hepatitis.
 Necessary emergency dental care should be provided with
the use of an isolated operatory and minimal aerosol
production.

48. CDC Guidelines for Exposure to Blood
 To reduce the risk of transmission of hepatitis viruses, the CDC has
published postexposure protocols for percutaneous or permucosal
exposure to blood.
 Implementation of these protocols is dependent on the virus
present in the source person and the vaccinated state of the exposed
person .
 A vaccinated individual who sustains a needlestick injury should be
tested for an adequate titer of anti-HBs if those levels are unknown.
 If levels are inadequate, the individual immediately should receive
an injection of HBIG and a vaccine booster dose
 If the antibody titer is adequate, nothing further is required.
 If an unvaccinated individual sustains an inadvertent percutaneous
or permucosal exposure to hepatitis B, immediate administration of
HBIG and initiation of the vaccine are recommended.

49.  Although no postexposure protocol or vaccine is available at
this time for HCV infection, current CDC guidelines
recommend that
1. the source person should receive baseline testing for anti-HCV
2. exposed persons should receive baseline and follow-up testing
at 6 months for anti-HCV and liver enzyme activity,
3. anti-HCV enzyme immunoassay positive results should be
confirmed by recombinant immunoblot assay (RIBA),
4. postexposure prophylaxis should be avoided with
immunoglobulin or antiviral agents,
5. health care workers should be educated regarding the risks
and prevention of bloodborne infection.

50. Exposure Control Plan
 With respect to hepatitis viruses, the U.S. Occupational
Safety and Health Administration mandates that
 all employers must maintain an exposure control plan
and must protect employees from the hazards of
bloodborne pathogens by applying standard precautions
and
 by providing the following as a minimum:
Hepatitis B vaccinations to employees
Postexposure evaluation and follow-up
Record keeping of exposures
Generic bloodborne pathogen training
Personal protective equipment at no cost to employees

51. Drug Administration
 No special drug considerations are required for a patient
who has completely recovered from viral hepatitis.
 However, if a patient has chronic active hepatitis or is a
carrier of HBsAg or HCV and has impaired liver function,
the dosage of drugs metabolized by the liver should be
decreased, or these drugs should be avoided, if possible as
advised by the physician.

52.  As a guideline, drugs metabolized in the liver should be considered for
diminished dosage
 when one or more of the following are present:
Aminotransferase levels elevated to greater than 4 times normal values
Serum bilirubin elevated to above 35 μM/L or 2 mg/dL
Serum albumin levels lower than 35 mg/L
Signs of ascites and encephalopathy, and prolonged bleeding time
 A quantity of three cartridges of 2% lidocaine (120 mg) is considered a
relatively limited amount of drug.

53.  Treatment planning modifications are not required for
the patient who has recovered from hepatitis.
 Oral Manifestations and Complications
 Abnormal bleeding is associated with hepatitis and
significant liver damage.
 This may result from
abnormal synthesis of blood clotting factors,
abnormal polymerization of fibrin,
inadequate fibrin stabilization,
excessive fibrinolysis, or
thrombocytopenia associated with splenomegaly that
accompanies chronic liver disease.

54.  • Before any surgery is performed, the platelet count should be
obtained, and it should be confirmed that the international
normalized ratio (INR) is lower than 3.5.
 If the INR is 3.5 or greater, the potential for severe postoperative
bleeding exists.
 In this case, extensive surgical procedures should be postponed.
 If surgery is necessary, an injection of vitamin K usually corrects the
problem and should be discussed with the physician.
 Chronic viral hepatitis increases the risk for hepatocellular
carcinoma.
 This malignancy rarely metastasizes to the jaw (fewer than 30 cases
in the jaw were reported)
 Oral metastases primarily present as hemorrhagic expanding
masses located in the premolar and ramus regions of the mandible.

55. REFERENCES
 Harrison's Principles of Internal Medicine
 Scully’s Medical problems in Dentistry 7th Ed
 Robbins and Cotran’s Pathologic basis of disease
 Viral hepatitis and the surgeon. HPB, 2005; 7: 56–64
 J Clin Exp Dent. 2011;3(2):e127-34. Dental treatment in patients with
liver disease