Dental considerations in patients with liver disease 2015 Oral health in patients with liver cirrhosis. Eur J Gastroenterol Hepatol.2015 Jul;27(7):834-9. doi: 10.1097/MEG.0000000000000356. Grnkjr LL1,Vilstrup H. Abstract OBJECTIVE:The aim of this study was to describe the oral care habits and self-perceived oral health in patients with liver cirrhosis, as well as to evaluate the impact of oral health on well-being and the relation to nutritional status.
PARTICIPANTS AND METHODS:From October 2012 to May 2013, we carried out a prospective study on patients with liver cirrhosis. Questions on oral care habits and self-perceived oral health were answered, and the Oral Health Impact Profile questionnaire (OHIP-14) provided information on oral conditions. The findings were compared with The Danish Institute for Health Services Research report on the Danish population's dental status.
RESULTS:One hundred and seven patients participated. Their oral care habits and self-perceived oral health were poorer than the Danish population; the patients had fewer teeth (on average 19 vs. 26, P = 0.0001), attended the dentist less frequently (P = 0.001), more rarely brushed teeth (P = 0.001) and had problems with oral dryness (68 vs. 14%, P = 0.0001). The patients' mean OHIP score was 5.21 7.2, with the most commonly reported problems being related to taste and food intake. An association was observed between the OHIP score and the patients' nutritional risk score (P = 0.01).
CONCLUSION:Our results showed that cirrhosis patients cared less for oral health than the background population. Their resulting problems may be contributing factors to their nutritional risk and decreased well-being. Oral health problems may thus have adverse prognostic importance. Our results emphasize the need for measures to protect and improve the oral health of cirrhosis patients.
Aug 18 2014 Getting Dental Work with Hepatitis C and Cirrhosis Getting Dental Work withHepatitis Cand Cirrhosis is important. A good dentist ..
2014 Oral Conditions Might Cause Severe Outcomes in Patients With Viral Hepatitis Infection Nima Mahboobi 1, * ; and Seyed Moayed Alavian 2 1 Department of Oral and Maxillofacial Surgery, Tehran University of Medical Sciences, Tehran, IR Iran2 Middle East Liver Diseases Center (MELD Center), Tehran, IR Iran *Corresponding Author: Nima Mahboobi, Department of Oral and Maxillofacial Surgery, Tehran University of Medical Sciences, Tehran, IR Iran. Tel: +98-2188989161, E-mail: nima.mahboobi@gmail.com. Hepatitis Monthly. 14(12): e25866 , DOI: 10.5812/hepatmon.25866 Article Type: Editorial; Received: Dec 8, 2014; Revised: Dec 8, 2014; Accepted: Nov 13, 2014; epub: Dec 25, 2014; collection: Dec 2014 Keywords: Health; Infection; Hepatitis
The world health organization (WHO) has defined health as a state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity. It is easy to express that complete health and wellness is merely impossible without oral health (1). After tooth decay in humans known as the most common infectious disease in the globe, periodontal diseases including gingivitis and periodontitis are among the most common oral diseases. The periodontal diseases are a group of chronic inflammatory diseases, involving the soft tissue and bone surrounding the teeth in the jaws, known as periodontium. Periodontal diseases are mainly caused by bacterial infection (2, 3). Although a review article published in 2008 showed a possible trend of a lower prevalence of periodontitis in the last 30 years, the authors of the paper recommended more research in the area to approve the evidence (4). To date, the association of various conditions and periodontal diseases has been acknowledged. A long list including overweight/obesity, hypertension, metabolic syndrome, diabetes mellitus, child preterm birth and low birth weight, rheumatoid arthritis and chronic obstructive pulmonary disease can be mentioned (5-7). Therefore, a hypothesis of association between either viral hepatitis infection or its progression and periodontal diseases seems quite close to mind. Previously, the association of several oral diseases including oral lichen planus, Sjogrens syndrome and pemphigus vulgaris with viral hepatitis infection was documented (8, 9).
A study performed by Nagao et al. (10) and published in the current issue is noteworthy from different aspects. Little has been dedicated to reveal the association between periodontal diseases and outcomes of viral hepatitis infection. According to their self-claimed statement of being the first study evaluating periodontal disease and patients with liver diseases resulting from viral hepatitis infection, the results were shocking. The conclusion states that periodontitis might be associated with progression of liver disease in patients with viral hepatitis, hence, control of oral diseases is essential for the prevention and management of liver fibrosis. This conclusion draws the attention of researchers to possible confounding factors never focused before. While performing different research projects on various links between hepatitis and dental setting in the past years, we reflected lack of data experience repeatedly. The conditions that made us urge researchers to develop research on oral fluid and viral hepatitis, viral hepatitis transmission risk during dental treatments and now the role of oral diseases on viral hepatitis have never been acknowledged. However, there are inconsistencies that must be noted before establishing new research. The methodology for studies on periodontal diseases remains elusive. A fundamental prerequisite for any epidemiological study is an accurate definition of the disease under investigation. Unfortunately in periodontal research, uniform criteria have not been established so far. Because of methodological problems the data used to assess treatment needs for periodontal diseases have been of questionable value and are not comparable (11). References and source
2012 Sept2012 Dental and Orofacial Health and Hepatitis CPrior to treating HCV it is important that any active dentaldisease be managed. Non-urgent dental treatment may need to be postponeduntil HCV treatment has ceased. Unfortunately, dental problems areknown to delay the onset of treatment for HCV. Dentaltreatment during anti-HCV therapy should be undertaken following consultation withmedical specialists. Blood tests and further investigations may beappropriate and in some cases in-patient care may be required. Immunocompromised patients, particularly those with neutropaenia, are at risk ofsepsis. If emergency dental treatment is necessary, consultation withmedical specialists is recommended. If the patient is anaemic, coagulopathic or thrombocytopaenic precautions may be needed. Pre-treatment optimisation and comprehensive post-operative care may berequired. Particular attention must be given to haemostasis....Download PDF Here..
Received:23/06/2010 Accepted: 16/01/2011
Abstract Introduction: Liver diseases are very common, and the main underlying causes are viralinfections, alcohol abuse and lipid and carbohydrate metabolic disorders. The liver has a broad range of functions inmaintaining homeos- tasis andhealth, and moreover metabolizes many drug substances. Objective: An update is provided on the oral manifestationsseen in patients with viral hepatitis, alcoholic and non-alcoholic liverdisease, cirrhosis and hepa-tocellular carcinoma, and on the dental management of such patients. Material and methods:
A Medline-PubMed search was conducted of the literature over the last 15 years using the keywords: hepatitis, alcoholic hepatitis, fatty liver, cirrhosis and hepatocellular carcinoma. A total of 28 articles were reviewed, comprising 20 lite- rature reviews,a clinical guide, three clinical trials and four case series.
Results: Oral clinical manifestations can be observed reflecting liver dysfunction, such as bleeding disorders, jaundice, foetorhepaticus, cheilitis, smooth tongue,xerostomia, bruxism and crusted perioral rash. In the case of infection causedby hepatitis C virus (HCV), the most frequent extrahepatic manifestations mostly affect the oral region in the form of lichen planus, xerostomia, Sjgrens syndrome and sialadenitis. The main complications of the patient with liverdisease are risk of contagion (for healthcarepersonnel and other patients), the risk of bleeding and the risk of toxicitydue to alteration of the metabolism of certain drugs.
Keywords: Hepatitis, alcoholic hepatitis, fatty liver, cirrosis, hepatocellular carcinoma. Cruz-Pamplona M,Margaix-Muoz M, Gracia Sarrin-Prez MG.Dentalconsiderations in patients with liver disease. J Clin Exp Dent. 2011;3(2):e127-34.
http://www.medicinaoral.com/odo/volumenes/v3i2/jcedv3i2p127.pdf Article Number: 50340 http://www.medicinaoral.com/odo/indice.htm Medicina Oral S. L. C.I.F. B 96689336 - eISSN: 1989-5488 eMail: jced@jced.es Introduction Liver diseases are very common and can beclassified as acute (characterized by rapid resolution andcomplete restitution of organ structure and function once theun-derlying cause has been eliminated) or chronic (charac- terized by persistent damage, with progressivelyimpai-red organ function secondary to the increase in livercell damage). Based on the extent and origin of thedamage, chronic liver disease ranges from steatosis or fatty liver to hepatocellular carcinoma, and includes hepatitis, fi-brosis and cirrhosis. Liver diseases can also beclassified as infectious (hepatitis A, B, C, D and E viruses, infec-tious mononucleosis, or secondary syphilis andtubercu- losis) or non-infectious (substance abuse such asalcohol and drugs, e.g., paracetamol, halothane, ketoconazole, methyldopa and methotrexate) (1).
The liver has a broad range of functions inmaintaining homeostasis and health: it synthesizes mostessential serum proteins (albumin, transporter proteins,blood coagulation factors V, VII, IX and X, prothrombin and fibrinogen (1), 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, cho- lesterol, amino acids), and metabolizes and conjugates lipophilic compounds (bilirubin, cations, drugs) to faci- litate their excretion in bile or urine.
Liverdysfunction alters the metabolism of carbohydrates, lipids,proteins, drugs, bilirubin and hormones (2). Accordingly, liver di- sease is characterized by a series of aspects that mustbe taken into account in the context of medical and dental care (3).
Since many drug substances are metabolized in the liver, it is essential for the clinician to compile a complete me- dical history, evaluating all body systems and themedi-cation used by the patient. The patient drug metabolizing capacity can be evaluated based on the analysis ofenzy-mes such as alanine aminotransferase (ALT) oraspartate aminotransferase (AST), and other liver functiontests (2, 4).
In situations of advanced liver disease, the vitamin K le-vels can be significantly lowered, thus giving rise to a re- duction in the production of blood coagulation factors. In addition, portal hypertension can scavenge platelets for- med in the spleen, thus giving rise to thrombocytopenia.This in turn can lead to an excessive bleeding tendency, which is one of the main adverse effects seen during the treatment of patients with impaired liver function (4). Dentists are particularly at risk of hepatitis B and Ccon- tagion, due to the transmission routes of these viruses, since these professionals are exposed to the bloodand oral secretions of potentially infected individuals (5) particularly in the case of accidents with sharp or cutting instruments.
VIRAL HEPATITIS Hepatitis of viral origin comprises aheterogeneous group of diseases caused by at least 6 different types of viruses: A, B, C, D, E and G (2).
Five million new cases of viral hepatitis are documented each year throughout the world, and a study published by Chandler-Gutirrez et al. (6) estimates the prevalence in Spain to be 3.7%. - Hepatitis A Hepatitis A is caused by the hepatitis A virus(HAV), an RNA picornavirus (3) endemic in many developing countries. Its estimated prevalence is 1.1% (6). This vi- rus is transmitted via the enteral (oral-fecal) route (5), as a result of the ingestion of contaminated water or food (mollusks), though intrafamilial contagion has also been described, as well as contagion in closed institutions and secondary to sexual intercourse.
The disease is typically mild and self-limiting, and is cha- racterized by the sudden onset of nonspecific symptoms. There is no carrier state. In children or young indivi- duals the disease tends to be asymptomatic, while adults typically present fever, fatigue, abdominal discomfort, diarrhea, nausea and/or jaundice. The patient is able to transmit the infection during the incubation period (2-6 weeks) and until the appearance of symptoms. The diagnosis is based on the signs and symptoms and on serological testing for anti-HAV IgM and IgG anti- bodies (3). Host response in the form of anti-HAV anti- bodies affords lifelong immunity, protecting the patient against future HAV infection.
The risk of nosocomial contagion among healthcare per- sonnel is quite low (3). Vaccines are available that offer immunity against HAV (Havrix, Vaqta) for people at risk (i.e., subjects traveling to endemic areas, drug abusers, patients with chronic liver disease and subjects with occupational risk factors) (2, 3). - Hepatitis B The hepatitis B virus (HBV) is an encapsulatedDNA virus that replicates within the hepatocyte (3). Hepatitis B is a worldwide health problem, with an estimated 400 million carriers of the virus (5). It has been calculated that 1.53% of all patients reporting to the dental clinic are HBV carriers (6). The transmission routes comprise sexual contact, intra- venous drug use and blood transfusions. In Asia perinatal transmission is common (3). An important consideration among dental professionals is the risk of percutaneous transmission through punctures or cuts with instruments infected from HBV-positive patients, or absorption through the mucosal surfaces (eyes, oral cavity). Trans- mission through saliva can occur as a result of absorp- tion from mucosal surfaces (2). Some studies have re- ported the presence of HBsAg in saliva and crevicular fluid of HBV-positive patients. Dental professionals, particularly those dedicated to oral surgery (7), have athree- to four-fold greater risk of HBV infection than the general population (3), though vaccines and barrier methods have contributed to lessen the risk (2, 7). Fo- llowing inoculation, the seroconversion risk is 30% (8). The incubation period lasts 2-6 months. Over 50% of all infections are subclinical and are not associated with jaundice. In this context, since the disease may prove asymptomatic, many people are unaware that they have suffered the infection in the past (5). Approximately 90% of all HBV-infected adults show complete healing, but 5-10% develop chronic hepatitis with complications in the form of cirrhosis and hepatocellular carcinoma (3, 4), resulting in 5000-6000 deaths a year due to liver fa- ilure (4).
The disease is diagnosed by quantifying the levels of HBV DNA, HBsAg and the antigen / antibody ratio. Vaccines have been developed that induce an effective immune response against the virus in most patients. If a non-immunized individual becomes exposed to HBV, immunoglobulincan be administered to afford protec-tion afterexposure. The current management protocols include HBV immunization as part of the pediatric vac-cinationprogram (3)
HepatitisC Hepatitis C virus (HCV) infection is the main cause of chronic liverdisease (9, 10) and of liver-related morbi-dity and mortality worldwide (9). It has been estimated that 8000 to10,000 deaths a year are attributable to HCV (4), and thelatter represents the main indication for li- ver transplantation in Europe and the United States (9).The estimatedglobal prevalence of the disease is 2.2%, representing approximately 130 million infected indivi-duals in the world (10). Great geographical variabilityis observed(9), possibly as a result of immunogenetic factors. Thelowest prevalences are found in the Uni- ted Kingdom and Scandinavia, and the highest in Egypt (11). HCV is an RNA virus mainly transmitted via the paren- teral routefrom infected blood (3, 9, 12). The sources of contagion include blood transfusion (although the risk has beenminimized since donor blood tests and controls are made (12)), percutaneous exposure through contami- natedinstruments, and occupational exposure to blood (9). The individuals at greatest risk are hemophiliacs,patients ondialysis and parenteral drug abusers.
Other transmission routes are sexual contact and perinatal and idiopathiccontagion (3). The prevalence of the infection among dentalprofessionals is similar to that found in the generalpopulation, though epidemiological studies suggest that dentists constitute a risk group for HCV in- fection (12). Following inoculation, the estimated seroconversion risk is 1.8% (8). The incubation period is long (up to three months), and 85% of all patients with HCV in- fection developchronic hepatitis. In those cases wheresymptoms areobserved, these tend to be mild, and most subjects remain relatively asymptomatic during the first two decades after infection with the virus (4). The morbidity associated to HCV infection is due not only to theconsequences of chronic liver disease but also to the extrahepatic manifestations (11). The best documented condition associated to hepatitis C is cryo- glubulinemia, a multisystemic disorder often characte- rized bypurpura, weakness and joint pain, and which may precede thedevelopment of B-cell non-Hodgkin lymphoma or membrane proliferative glomerulonephri- tis (12).
Otherrelated disorders are porphyria cutanea tarda, lichenplanus, sialadenitis, thyroid gland dys-function, diabetes mellitus and peripheral neuropathy (11). Over 74% of all HCV-infected patients ultimately developextrahepatic manifestations in the course of theinfection (10).
Different enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA) techniques have been developed for the diagnosis of HCV infection, though thediagnostic gold standard remains detection of the viral genome using real time polymerase chain reaction (RT-PCR) technology (3, 12). No effective vaccine against HCV has yet been deve- loped, and spontaneous resolution is unusual (12). The existing therapy comprises combination treatment with interferon and ribavirin, which offers a sustained res- ponse rate of 30-40% (3). CHRONIC HEPATITIS Chronic hepatitis is a diffuse inflammatory disorder of the liver witha duration of over 6 months in which the underlying cause can be infectious (mainly hepatitis C virus and, to a lesser extent, hepatitis B and D viruses), pharmacological or immunological. The disease can develop in the absence of symptoms or withnonspecific manifestations such as fatigue, nausea or abdominal pain. The course is normally slow and pro- gressive, and symptoms typically do not manifest until years after the initial causal event (e.g., infection). Some patientsdevelop the disorder without significant liver damage, while others rapidly progress towards cirrhosis and possible hepatocarcinoma. Chronic hepatitis due to HCV infection is the principal cause of cirrhosis and he- patocellular carcinoma (3).
ALCOHOLIC LIVER DISEASE Alcoholic liver disease is one of the 10 most common causes of death in the industrialized world, and is res- ponsible for 3% of all fatalities. The epidemiological data indicate a threshold of 80 g of alcohol in males and 20 g infemales, consumed on a daily basis during 10-12 years, in order to cause the corresponding liver damage. Ten grams of pure ethanol are equivalent to a glass of wine or a beer,while a glass of whiskey doubles that amount. Factors such as chronic hepatitis C infection, obesity andgenetic factors can accelerate the develop
NON-ALCOHOLIC FATTY LIVER Non-alcoholic fatty liver is defined as the accumulation of fat (mainly triglycerides) in the liver, representing over 5% of the weight of the organ (5), in the absence of alcohol consumption in excess of 10 g a day (15).The observedliver damage ranges greatly from simple steatosis (accumulation of fat in the liver) to steatohepatitis(fat accumulation with added inflammation), advan- ced fibrosisand cirrhosis (16). This disorder is mainly associated to obesity, diabetes, hyperlipidemia and insulin resistance. There is a strong correlation between insulin resistance and excessive triglyceride accumulation within the liver cells (15). However, 16.4% of all patients with non-alcoholic fatty liver presentnone of these predisposing factors (17) The condition ispotentially reversible after eliminating or minimizingthe aforementioned causal factors (14). No clear treatments have been established to date for non-alcoholic fatty liver, though interventions such as bariatricsurgery (in the case of obese individuals) and oral antidiabetic drugs (glitazones) in patients with type 2 diabetes have shown encouraging results (15).
CIRRHOSIS Liver cirrhosis is very common in our setting, with well defined morphopathological characteristics that lead to destruction of the liver parenchyma. The disease is accompanied by a series of extrahepatic manifestations in other body organs and system (18). Liver cirrhosis is irreversible, and is characterized by the formation of fibrous scarring in the liver, with the formation of rege-neration nodules that increase resistance to blood flow through theorgan. The resulting deficient liver perfu- sion damages vital structures in the organ and adversely affects its physiological functions (19). The main cau-ses of liver cirrhosis are hepatitis B and C infection and alcohol abuse.Other potential causes are non-alcoholic steatohepatitis, genetic alterations and autoimmune di-sorders (3). The maincomplications of cirrhosis are portal hyperten- sion,hepatocellular carcinoma and organ function loss. Cirrhosis in itself constitutes a risk factor for the develo- pment of hepatocellular carcinoma (16). The treatment options comprise suppression of the cau- sal stimulus, antiviral therapy and liver transplantation in the endstages of cirrhotic disease (3).
HEPATOCELLULAR CARCINOMA Hepatocellularcarcinoma is the fifth most frequent can-cer worldwide (16). As such, it constitutes an important public health problem, and is one of the most common and life-threatening malignancies in the world with a survival rate after two years of only about 2% (3). It has been estimated that HBV and HCV are responsible for over 80% of all hepatocarcinomas. The other cau- ses are alcoholic and non-alcoholic steatohepatitis. Most patients with hepatocellular carcinoma have a history of cirrhosis, which in itself constitutes a preneoplastic con- dition (12, 16). Liver cirrhosis has a prolonged natural course, and pro- duces symptoms only in the advanced stages of the di-sease, when no healing treatment options are available. The main treatment for hepatocellular carcinoma is sur- gery (in thosecases where the tumor proves resectable), though unfortunately many cases are non-operable due to theproximity of vital structures, the presence of me- tastases, or other comorbidities (3). Objectives The present study offers a literature review of the oral manifestations that can be found in patients with viral hepatitis, alcoholic and non-alcoholic liver disease, cirr- hosis and hepatocellular carcinoma, and the dental ma-nagement of patients with these liver disorders.
Material and Methods A literature search was made of the articles indexed in the PubMed Medline database, using the following MeSH validated key words: hepatitis, alcoholic hepati- tis, fatty liver, cirrhosis and hepatocellular carcinoma. The search was limited to articles in English or Spanish published overthe last 15 years. A total of 28 articles were reviewed, comprising 20 literature reviews, a clini- cal guide, three clinical trials and four case series.
Results 1. ORALCLINICAL MANIFESTATIONS The oral cavity can reflect liver dysfunction in the form of mucosal membrane jaundice, bleeding disorders, pe-techiae, increased vulnerability to bruising, gingivitis, gingival bleeding (even in response to minimum trau-ma) (3, 19),foetor hepaticus (a characteristic odor of advanced liver disease), cheilitis, smooth and atrophic tongue, xerostomia, bruxism and crusted perioral rash (1).
In these patients, chronic periodontal disease is a common finding. Patients with alcoholic hepatitis can present glossitis, angle cheilitis and gingivitis, particularly in combination withnutritional deficiencies (3, 20). Some patients who consume largeamounts of alcohol for prolonged periods of time can develop sialadenosis. As commented by Frie- dlander (20), this is believed to be the result of ethanol- induced peripheral autonomic neuropathy giving rise to alterations insalivary metabolism and secretion.
Patients with advanced cirrhosis tend to present defi-cient oral hygiene, particularly in those cases where the liver impairment is associated to alcohol abuse. Bagn et al. (18) reported worsened dental conditions in patients with livercirrhosis, in coincidence with other authors such as Novacek et al. (21), who considered that due to the severity and characteristics of cirrhosis, patients tend to neglect care of the oral cavity (18). In a recent study, Grossmann et al (9). found many patients with HCV infection to present poor dental health a situation that contributes to worsen their quality of life. Extrahepatic manifestations have been reported in 74% of all HCV-infected individuals (19), and some of these conditions predominantly or exclusively affect the oral region (10). The main disorders associated with HCV infection are xerostomia, Sjgrens syndrome (SS), sia-ladenitis and particularly lichen planus (LP) (9). Xerostomia increases patient vulnerability to caries andoral softtissue disorders (9) 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 Sjgrens syndrome or whether itis directly responsible for development of Sjgrens syndrome in certain types of patients. Howe-ver, it isnotorious that some subjects can present a triple association of HCV infection, Sjgrens syndrome and sialadenitis orsalivary gland lymphoma (10).
Although bacteria are the main cause of sialadenitis, vi- ruses such as HCV have been implicated as causes of sialadenitis associated to xerostomia (19). Epidemiological evidence suggests that lichen planus may be significantly associated to HCV infection, though the existing data are controversial (22). This association appears to be dependent upon the geographical setting, being more common in Mediterranean countries and in Japan (22). Bagn et al. (23) found the prevalence of HCV infection to be greater in patients with oral lichen planus (OLP) than in the control group. Although further studies are needed, recent data suggest that patients are most likely first infected with HCV and posteriorly de- velop lichen planus (24) though the way in which this
2. DENTAL MANAGEMENT
Liver disease has important implications for patients receiving dental treatment (3). The most frequent pro-blems associated with liver disease in clinical practice refer to the risk of viral contagion on the part of the den-tal 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 subs-tances (1) which increases the risk of toxicity. HCV has been detected on different surfaces within the dental clinic after treating patients with hepatitis C, and the virus moreover is able to remain stable at room tem-perature for over 5 days (12). Strict sterilization mea-sures are therefore required, since deficient sterilizationcan expose both the dentist and other patients to hepa-titis infection (5). The universal protective measures areapplicable in order to prevent cross-infection, i.e., theuse of barrier methods, with correct sterilization and di-sinfection measures (1). It has been demonstrated thatconventional sterilization techniques eliminate specificproteins and nucleic acids (HBV DNA and HCV RNA)from dental instruments previously infected with HBVand HCV.
x
Although there are no data confirming theirefficacy in lessening the risk of contagion, the measuresre commended in the case of accidental perforation of the skin with instruments or needles comprise careful was-hing of the wound (without rubbing, as this may inocula-te the virus into deeper tissues) for several minutes withsoap and water, or using a disinfectant of established efficacy against the virus (iodine solutions or chlorine formulations). In turn, pressure should be applied benea-th the level of the wound in order to induce bleeding and thus help evacuate any possible infectious material.If exposure through some mucosal membrane has oc-curred, abundant irrigation with tap water, sterile saline solution or sterile water is advised, for several minutes. The rationale behind these measures is to reduce the number of viral units to below the threshold count nee-ded to cause infection (i.e., the infectious dose). In this sense, dilution with water may lower the viral count to below this threshold (8). Whenever possible, the hepa-titis antigen status of the patient should be determined.In the event of parenteral exposure to hepatitis virus-positive antigens, the dentist should receive treatment with anti-hepatitis B immunoglobulin (5). Table 1 offers a schematic description of the steps to be followed. The compilation of a detailed clinical history is essen-tial before dental treatment in order to identify patientsposing possible risks (5), together with a thorough oralexploration. Interconsultation with the patient physicianor specialist is advisable in order to establish a safe andadequate treatment plan adapted to the medical condi-tion of the patient (3), considering the degree of liver functional impairment involved (1).
Table 1
x
Exploration of the oral cavity should assess any signs alerting to the exis-tence of systemic disease. The patient should receive an explanation of the risks associated with treatment, and informed consent is to be obtained.In patients with acute-phase viral hepatitis, only emer-gency treatment should be considered. In subjects with chronic hepatitis it is important to determine the pos-sible existence of associated disorders (autoimmuneprocesses, diabetes, etc.) in order to prevent their direct complications and problems derived from specific me-dication use (corticosteroids and/or immune suppres-sors). Evaluation is also required of the possible medical conditions associated to HCV contagion, fundamentally blood transmitted infections (HIV, HBV).It also must be taken into account that liver disease is often associated with a decrease in plasma coagulation factor concentrations (2, 3). In a patient with liver di-sease, the surgical risk is related to the severity of the disease, the type of surgery planned, and the presence of comorbidities. Surgery is contraindicated in patients with certain conditions such as acute hepatitis, acute li-ver failure or alcoholic hepatitis (25). If invasive mea-sures are required, prior coagulation and hemostasistests are required: complete blood count, bleeding time,prothrombin time / international normalized ratio (INR),thrombin time, thromboplastin time and liver bioche-mistry (GOT, GPT and GGT) (1, 26). Table 2 reports the normal coagulation test values. In the event altered test values are detected, the hematologist or liver spe-cialist should be consulted (3), with the postponement of elective treatment. Any emergency treatments should be provided in the hospital setting.
In the event of surgery, trauma should be minimized (3) in order to optimize hemostasis, with a careful surgical technique,applying pressure to control bleeding and using hemos-tatic agents (2). Based on the laboratory test findings and the treatment to be carried out, local hemostatic agents may be advisable (oxidized and regenerated cellulose),as well as antifibrinolytic agents (tranexamic acid), fresh plasma, platelets and vitamin K (1, 26). Antibiotic pro-phylaxis is suggested, since liver dysfunction is associa-ted to diminished immune competence (2).Liver disease may result in alterations in the metabolism of certain drugs. The physician treating the patient the-refore should be consulted in order to establish which drugs are used, their doses and possible interactions(3). The administration of certain analgesics, antibioticsand local anesthetics is generally well tolerated by pa-tients with mild to moderate liver dysfunction, though modifications may prove necessary in individuals with advanced stage liver disease (2). In this context, drugs metabolized in the liver may have to be used with cau-tion or their doses reduced (1, 26) (Table 3), and certain substances such as erythromycin, metronidazole or te-tracyclines must be avoided entirely (3). Most of the an-tibiotics prescribed for oral and maxillofacial infections can be used in patients with chronic liver disease, and in general the beta-lactams can be administered. Amino-glycosides can increase the risk of liver toxicity in pa-tients with liver disease, and so should be avoided. Themetabolism of clindamycin in turn is prolonged in suchpatients, and different studies suggest that it contribu-tes to liver degeneration (27).
Nonsteroidal antiinflam-matory drugs (NSAIDs) should be used with caution oravoided, due to the risk of gastrointestinal bleeding andgastritis usually associated to liver disease. Prophylaxiscan be provided in the form of antacids or histamine re-ceptor antagonists (2, 3). Acetaminophen (paracetamol)is to be avoided in patients with serious liver disease (4),and aspirin and NSAIDs are not indicated in patientswith altered hemostasis (4). Authors such as Douglas etal. (27) describe acetaminophen as a safe alternative toaspirin or NSAIDs that can be administered at doses ofup to 4 g/day during two weeks without adverse liver effects, warning patients to avoid alcohol consumption while receiving treatment with the drug. In patients using benzodiazepines, the dose should be lowered, withprolongation of the interval between doses. Local anes-thetics are generally safe provided the total dosage doesnot exceed 7 mg/kg, combined with epinephrine (27).Table 4 shows the drugs that are contraindicated and those that can be used with caution. Although some of these substances are metabolized in the liver, the doses at which they are used in dental practice are considered to be acceptable unless the patient suffers very severe liver dysfunction.
Table 4 shows the drugs that are contraindicated and those that can be used withcaution.
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