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World J Gastroenterol. Jun 28, 2014; 20(24): 7534-7543
Published online Jun 28, 2014. doi: 10.3748/wjg.v20.i24.7534
Oral manifestations of hepatitis C virus infection
Marco Carrozzo, Kara Scally, Centre for Oral Health Research, Oral Medicine Department, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4BW, United Kingdom
Author contributions: Carrozzo M collected the underlying material and wrote the initial draft of the manuscript; Scally K finalized and revised the manuscript; all authors have read and approved the final version of the manuscript.
Correspondence to: Marco Carrozzo, MD, DSM (Turin 1995), Professor of Oral Medicine, Centre for Oral Health Research, Oral Medicine Department, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne NE2 4BW, United Kingdom. marco.carrozzo@ncl.ac.uk
Telephone: +44-191-2227818 Fax: +44-191-2226137
Received: October 13, 2013
Revised: January 21, 2014
Accepted: March 19, 2014
Published online: June 28, 2014

Abstract

Extrahepatic manifestations (EHMs) of hepatitis C virus (HCV) infection can affect a variety of organ systems with significant morbidity and mortality. Some of the most frequently reported EHM of HCV infection, involve the oral region predominantly or exclusively. Oral lichen planus (OLP) is a chronic inflammatory condition that is potentially malignant and represents cell-mediated reaction to a variety of extrinsic antigens, altered self-antigens, or super antigens. Robust epidemiological evidence support the link between OLP and HCV. As the virus may replicate in the oral mucosa and attract HCV-specific T lymphocytes, HCV may be implicated in OLP pathogenesis. Sjögren syndrome (SjS) is an autoimmune exocrinopathy, characterized by dryness of the mouth and eyes and a multitude of other systemic signs and symptoms. SjS patients have also an increased risk of non-Hodgkin lymphoma. Patients with chronic hepatitis C do frequently have histological signs of Sjögren-like sialadenitis with mild or even absent clinical symptoms. However, it is still unclear if HCV may cause a disease mimicking SjS or it is directly responsible for the development of SjS in a specific subset of patients. Oral squamous cell carcinoma is the most common oral malignant tumour and at least in some part of the world could be linked to HCV.

Key Words: Hepatitis C virus, Lichen planus, Oral lichen planus, Sjogren’s syndrome, Sialadenitis, Oral squamous cell carcinoma

Core tip: Hepatitis C virus can be frequently associated with potentially malignant and malignant oral diseases and could be a triggering factor of some of those disorders or at least influence their outcome. The association is very robust for oral lichen planus, while for Sjogren’syndrome it is strongly suspected and in oral squamous cell carcinoma indicated by recent large epidemiological data.



INTRODUCTION

Hepatitis C virus (HCV) is one of the major causes of chronic liver disease worldwide as the global estimated prevalence of HCV infection is 2.2%, representing approximately 170 million infected people worldwide. The lowest prevalence of anti-HCV antibodies (0.01%-0.1%) is in the United Kingdom and Scandinavia, whereas the highest prevalence is reported in Egypt (15%-20%) and intermediate rates (1.5%-3.5%) are found in United States, Japan, Spain and Italy[1]. An estimated 27% of cirrhosis and 25% of hepatocellular carcinoma worldwide occur in HCV-infected patients[2] .

Extrahepatic manifestations (EHMs) of HCV infection were first reported in the early 1990s[3] and can affect a variety of organ systems with significant morbidity and mortality. Forty to 75% of patients with chronic HCV infection exhibit at least one clinical EHM[3,4].

Because of the paucity of specific symptoms and signs caused by HCV, EHM could represent the first signal of this infection. Moreover, extrahepatic tissues might act as reservoir for HCV and this may have a profound effect on HCV transmission, morbidity and treatment[5].

The association of some EHM with HCV is very close, while for others it is strongly suspected and in other cases only slightly indicated by anecdotal data[6]. Some of the most frequently reported EHM of HCV infection, involve the oral region, predominantly or exclusively. The present review aims to report an update on these disorders.

ORAL LICHEN PLANUS

Lichen planus (LP) is an inflammatory mucocutaneous condition which most commonly affects middle-aged adults of both sexes, with a slight predominance in women[7]. The prevalence of skin lichen planus is unknown, but it is estimated to occur in < 1% of the population. It is thought to be significantly less frequent than exclusive oral LP (OLP) that affects approximately 1%-2% of the population[8]. Whereas in the majority of instances cutaneous lesions of LP are self-limiting and cause itching, lesions in OLP are chronic, rarely undergo spontaneous remission, are potentially malignant, rarely undergo spontaneous remission and are frequently a source of morbidity[7,9].

A large body of evidence supports a role for immune dysregulation in the pathogenesis of LP, specifically involving the cellular arm of the immune system[7,10]. Probably, LP is a stereotype cell-mediated reaction to a variety of extrinsic antigens, altered self-antigens, or super antigens. Among the extrinsic factors, several infective agents including some viruses and Helicobacter pylori have been linked with LP but apparently on the basis of equivocal data[7]. An association between LP and HCV was first reported in 1991, whereas the first OLP cases possibly linked to HCV were published in 1994[11,12]. Case-control studies from around the world produced seemingly contradictory evidence about the validity of the association.

Three recent independent meta-analyses[13-15] provide robust evidence that LP and HCV are associated (Table 1). The pooled OR and 95%CI of HCV exposure in LP patients vs controls ranged from 2.8 (95%CI: 2.4-3.2) to 5.4 (95%CI: 3.5-8.3) mainly because of differences in statistical methods and study inclusion criteria (Table 1). A similar OR of having LP was found in HCV patients vs controls[13,14]. The positive association was noted in studies across all the world but was more evident in East, Southeast Asia and South America and in Mediterranean countries[16]. Subgroup analyses[13,14] indicated that OLP was strongly associated with HCV (OR = 5.6, 95%CI: 3.5-8.8 and OR = 4.8, 95%CI: 3.0-7.7, respectively). The association between the isolated cutaneous type of LP and HCV was heavily skewed toward a positive association (OR = 10.2, 95%CI: 0.4-274)[13].

Table 1 Main summary of the recent 3 meta-analyses on lichen planus and hepatitis C virus.
Ref.CountryPeriod covered by searchType of studies includedStudies included in the meta-analysisCases/controlsMain resultsQuality assessment of the included studies
1Quality assessment of the systematic review process
Tool used
Shengyuan et al[15]ChinaNACase control or control-existing studies7024987/65022The prevalence of HCV exposure among patients with LP was higher than in control participants (OR = 5.4; 95%CI: 3.5-8.3)YesAccording to Robinson et al[17]High
Clinical or histological LP diagnosis58 on HCV prevalence in LP35570/139120The risk of LP among patients with HCV was higher than compared controls (OR = 2.5; 95%CI: 2.0-3.1)
HCV status diagnosed by serology or PCR12 on LP prevalence in HCV+
Lodi et al[13]ItalyJan 1966-Nov 2007Controlled studies3922544/2860LP patients have significantly higher risk than controls of being HCV seropositive (OR = 4.85; 95%CI: 3.58-6.56)YesCharacteristics of the study group, appropriateness of the control group, prospective designHigh
Clinical and histological LP diagnosis33 on HCV prevalence in LP; 6 on LP prevalence in HCV+3955/1242HCV patients have an increased risk of having LP (OR = 4.47; 95%CI: 1.84-10.86)
HCV status diagnosed by serology
Petti et al[14]ItalyNACross-sectional or case- control studies44NAThe overall risk for OLP among anti-HCV positive subjects was significantly higher than controls (OR = 2.8; 95%CI: 2.4-3.2)NoNAUncertain
Clinical or histological LP diagnosis. Any HCV testingThe fraction of global OLP cases associated with HCV (population attributable fraction) was 2.1% (95%CI: 1.9%-2.2%)

The putative pathogenetic link between OLP and HCV is still under investigation but molecular mimicry between the virus and host epitopes is unlikely, as well as viral factors such as genotype or viral load[19]. Clinically and histologically, HCV-related OLP is the same as “idiopathic” OLP[20], however the Th1 cytokine environment sustaining the oral lesions may be due to the HCV immunologic pressure and not genetically driven, as in idiopathic OLP[21].

Notably, HCV may replicate in the oral mucosa and may attract specific T cells. Indeed, in situ hybridization and extractive polymerase chain reaction (PCR) techniques revealed the presence of replicative intermediate HCV-RNA in skin and oral mucosa from patients with LP (Table 2). When high quality techniques were employed, positive and negative strands were detected by PCR in 75%-100% and 21%-100% of LP tissue specimens respectively and generally were more commonly found in OLP specimens (Table 2).

Table 2 Hepatitis C virus detection in lichen planus lesional tissue n (%).
CountryRef.nPatients HCV positivePatients with oral lesionsDetection of HCV in specimens of lichen planusTissue sampleTechniqueRatio of +/- strandsOral mucosa/skin HCV RNA
Genomic strandNegative strand
ItalySansonno et al[22]70NA0 (0)FreshIHC---
Mangia et al[23]191900 (0)FreshrTth RT-PCR---
Carrozzo et al[24]12121210 (83)FreshrTth RT-PCR, SA, PhA1-64 Various10 (83)4 (33)
Pilli et al[25]4443 (75)FreshrTth RT-PCR-3 (75)0 (0)
Femiano et al[26]2525250 (0)UnclearRT-PCR-0 (0)NA
JapanNagao et al[27]14141413 (93)FreshPCR, SA-13 (93)3 (21)
Kurokawa et al[28]3323 (100)FreshrTth RT-PCR-3 (100)3 (100)
SpainArrietaet al[29]23232323 (100)paraffin-embeddedISH-23 (100)23 (100)
Lazaro et al[30]5505 (100)paraffin-embeddedISH, IHC-5 (100)5 (100)
TurkeyErkek et al[31]5545 (100)paraffin-embeddedRT-PCR-5 (100)NA
United KingdomRoy et al[32]270270 (0)NART-PCR-0 (0)NA
Boyd et al[33]272NA0 (0)paraffin-embeddedIHC---
United StatesHarden et al[34]4410/0paraffin-embeddedRT-PCR-0 (0)NA
TotalOLP (%)8556 (66)5632 (58)
LP (%)217 (33)76 (85)

Pilli et al[25] found HCV specific CD4+ and CD8+ T cells more readily in oral lesional biopsy specimens than peripheral blood in LP patients with HCV infection. CD4+ T cell clones present in the oral mucosa showed a different T-Cell Receptor-Vb chain usage than those circulating in the peripheral blood, suggesting a specific compartmentalization at the site of the OLP lesions. Contrarily, HBV-specific T cells could not be found in the oral mucosa of patients with OLP and chronic HBV infection even if they were detectable in the peripheral blood[25]. This suggests that HCV-specific T cells among the lichen-infiltrating lymphocytes were not recruited as a result of the liver inflammation and may play a role in the pathogenesis of some OLP cases.

In conclusion, there is quite strong and convincing evidence that HCV is associated with OLP and possibly involved in its pathogenesis whereas similar evidence is not completely available for skin LP.

It would be thus prudent to at least ask OLP patients whether they have risk factors for having HCV and to screen those with significant risk with an ELISA for HCV antibodies[16]. However, risk factors for HCV acquisition differ substantially among countries and sometimes within the same country (for example in Italy). Indeed, whereas intravenous drug use accounted for 92.5% of infections in United Kingdom, it was the cause of transmission in just 27.8% of the cases in Italy where nosocomial infections were frequent, particularly in the south[35]. Moreover, some risk factors, for example dental procedures, seem to be peculiar to some countries like Spain, Romania and Turkey[35].

Because there is some evidence that OLP-HCV-ve+ patients might be at higher risk of malignant transformation[9] (see also below) and that anti-HCV treatment [particularly interferon alpha (IFN-α)] could worsen or even trigger OLP[36,37], it could also be worthwhile to screen HCV-ve+ patients for OLP presence. Individual screening strategies may need although to be developed in different countries to identify high risk patients.

SJOGREN-LIKE SIALADENITIS

Sjögren syndrome (SjS) is an autoimmune exocrinopathy, characterized by dryness of the mouth and eyes resulting from a chronic, progressive loss of secretory function of the salivary and lacrimal glands[38]. SjS can cause consistent oral and dental findings: increased caries rate, mucosal dryness, soreness, increased infections (both fungal and bacterial), altered properties of saliva (thicker, opaque, or viscous secretions), and enlargement of the salivary glands[38]. But, SjS is also associated with systemic visceral involvement, including pneumonitis, renal tubular acidosis, pancreatitis, myositis, and occasionally lymphocytic proliferation and a variety of neurological complications[39-41]. Patients with SjS have an excess mortality caused by haematological cancer, particularly non-Hodgkin lymphomas[42].

The pathogenesis of SjS is not completely clear but is generally considered to be a consequence of autoimmunity because of the presence of characteristic autoantibodies against RNA-binding proteins Ro and La and upon the observation of inflammatory infiltrates in the affected exocrine glands[38]. However, triggering factors are poorly understood but viral infections are highly regarded[38].

Diagnosis of SjS can be challenging, particularly in mild cases and still the discrepancy in diagnostic criteria led to substantial confusion in research publications and clinical-trial reports[38-43].

The first study reporting an association between salivary gland disorders and hepatitis C was published in 1992 and found that 57% of HCV- associated chronic liver disease patients exhibited characteristic SjS histological changes in the salivary glands[44]. Subsequent studies noted that, in contrast to SjS, lymphocytic infiltration in HCV+ve patients was pericapillary rather than periductal, with no destruction of the SG ducts, and that lymphocytic capillaritis resembled an early stage of disease[45].

Further studies[3,4,44-56] have shown controversial results but up to 80% of HCV-infected individuals may have some salivary or lacrimal abnormality, frequently represented by histological signs of mild sialadenitis. However, clinical evidence of dry mouth and mainly of dry eyes is often absent[57,58].

Several studies seem indeed to indicate that this sialadenitis may be significantly different from that of SjS. There is no female predominance, no specific antinuclear anti-Ro and anti-La antibodies, a frequent association with the HLA-DQB1*02[59] rather than with HLA-DR3 allele, milder histopathology (with a CD8+ rather than a CD4+ T-cell predominance), and apparently fewer clinical symptoms[45,48,58] (Table 3). On the other hand, from 0% to 19% of patients with frank SjS can be HCV-infected, the frequency varying with the geographical region, the HCV test and the SjS diagnostic criteria used (Table 4)[6]. The confusion about epidemiological data is enhanced by the fact that whereas the most recent American-European classification criteria for SjS the presence of HCV is considered an exclusion criterion[83,85], the term of “SjS-secondary to HCV” has been proposed for those patients with chronic HCV infection who fulfil the same criteria[86].

Table 3 Main clinical, serological, histological, genetic differences between sialadenitis in Sjogren’s syndrome and hepatitis C virus +ve patients.
VariableSjögren's syndromeHepatitis C virus
Sicca symptomsCommonly presentUsually absent or modest
Parotid swellingModerate to severeMild to moderate
Extra-glandular manifestationsMainly pulmonary, gastrointestinal, renal, and neurologic involvementMainly gastrointestinal and musculo-skeletal involvement
HistologyPeriductal lymphocytic infiltrationPericapillary lymphocytic infiltration
Infiltrating lymphocytic phenotypePredominantly CD4+ T cellsMixed CD4+/CD8+ T cells
AutoantibodiesHigh-frequency RF, ANA, anti-Ro/SSA and anti-La/SSB, alpha-fodrin antibodiesHigh frequency of RF, ANA, alpha-fodrin, low prevalence of anti-Ro/SSA and anti-La/SSB antibodies, high frequency of cryoglobulins
HLA associationB8, DR2 and DR3DQB1*02
LymphomagenesisPreferentially affecting salivary glandsAffecting both liver and salivary glands
Table 4 Prevalence of hepatitis C virus infection in patients with Sjögren’s syndrome.
CountryRef.nSjS Diagnostic CriteriaHCVve+ (%)
Francede Bandt[61]20NA10
Loustaud-Ratti et al[56]26NA8
Mariette et al[62]201Fox I10
Barrier et al[63]22NA9
Vidal et al[64]281Fox I14
Wattiaux et al[65]109European3
Boscagli et al[50]23NA5
Jorgensen et al[66]62European19
GermanyPotthoff et al[67]732AECG18
GreeceVitali et al[68]22Vitali5
HungarySzodoray et al[69]213European6
IndiaWanchu et al[70]23European4.4
ItalyAceti et al[71]261Fox I0
Vitali et al[68]44Vitali5
Frisoni et al[72]26NA4
Ceribelli et al[73]3052AECG3
JapanMasaki et al[74]98NA11
SpainGarcía-Carrasco et al[75]90European14
Coll et al[76]31European10
Fernandez-Campillo et al[77]26European19
Selva-O’Callaghan et al[78]98European7
SwedenVerbaan et al[52]53Copenhagen2
United KingdomPorter et al[79]18European0
United StatesKing et al[80]44NA0
United StatesMarrone et al[81]1003Fox II1

Available data on direct HCV replication of SGs are also scanty and controversial[51,52,87-90] and two recent studies suggest that sialadenitis in patients with chronic hepatitis C is not directly related to HCV[91,92].

An animal model of transgenic mice carrying the HCV envelope genes E1 and E2 has been constructed[93]. The mice developed an exocrinopathy involving the SGs and lachrymal glands (LGs) in 84% of cases. Initially, pericapillary lymphocytes were found, but soon focal infiltrates of small lymphocytes appeared, closely resembling sialadenitis noted in humans[44,93]. Nests of lymphatic infiltrates were also noted in the LGs, but they occurred later and were less extensive than those found in the SGs. This mode clearly suggests a possible direct role of the viral proteins in the pathogenesis of HCV-related sialadenitis. The pathogenesis of this sialadenitis in transgenic mice is however unclear: it seems indeed unlikely to be induced by an immune reaction against ductal cells expressing viral antigens, as only one out of 20 transgenic mice showed a weak antibody reaction to E1 protein[93].

Interestingly, human La antigen (also called SS-B) which is an RNA-binding protein of 50/52-kDa, and is a typical target of SjS-autoantibodies, plays a functional role in internal initiation of translation of the polyproteins of the HCV RNA stimulating HCV internal ribosome entry site-mediated translation[94,95]. La protein is a potent regulator and enhancer of HCV replication[96] and the expression of this autoantigen is significantly reduced after the administration of IFN-α in a dose-dependent manner. However, there are no studies on the role of La in HCV-related sialadenitis. Data about the effects of anti-HCV treatment on sicca symptoms are also patchy and controversial[97,98].

In conclusion, the epidemiologic and pathogenetic role of HCV in SjS development and the characteristics distinguishing classic SjS from HCV-related sialadenitis are still controversial and further studies are clearly warranted. The virus could cause a disease mimicking primary SjS or alternatively HCV might be directly responsible for the development of SjS in a specific subset of patients. Some patients may present a triple association between HCV, SjS-like sialadenitis and salivary glands lymphoma and the virus may be involved in the lymphomagenesis[99].

ORAL SQUAMOUS CELL CARCINOMA

Oral cavity cancer comprises of 2% to 3% of all malignancies and oral squamous cell carcinoma (OSCC) is the most common type of oral malignant tumours[100]. The identified risk factors of OSCC include tobacco use, alcohol consumption, chewing of betel leaves and areca nuts, low socioeconomic status[100]. Also viruses are supposed to potentially be involved in oral carcinogenesis[100,101].

Six human viruses have been considered by the International Agency for Research on Cancer as being carcinogenic based on sufficient evidence supporting their etiologic association with human cancers: they are Epstein-Barr virus, HBV, several types of human papilloma virus (HPV), human T-cell lymphotropic virus type 1, HCV, and Kaposi’s sarcoma-associated herpesvirus[102].

Oral verrucous and squamous cell carcinomas have been reported in HCV-infected patients with or without OLP[9,103-109], although the epidemiological relevance of this observation is unclear and HCV is a common cause of liver cirrhosis, which may itself represent an independent risk factor for the development of oral cancer[110].

Apart from OLP, HCV prevalence is generally not increased in patients with other potentially malignant oral lesions such as leukoplakia or dysplasia[111-113].

A study conducted at a veterans administration medical centre in New Orleans reported that 21.2% of 99 patients with squamous cell carcinoma of the head and neck were co-infected with HCV, which was significantly higher than previously published data (9.9%) (P = 0.004)[114]. Contrarily, in another study from Japan assessing the prevalence of HCV in 4402 patients requiring oral surgery, HCV antibody was more prevalent in patients with oral cavity cancer than in those with impacted teeth (OR = 2.433; P = 0.05), but this difference was reversed after age adjustment (OR = 0.443; P = 0.05)[115].

Recently, a nationwide, population-based, cohort study from Taiwan reported that the incidence of oral cavity cancers was 2.28-fold higher among patients with HCV alone than non-viral hepatitis group (6.15 vs 2.69 per 10000 person-years). After adjusting for socio-demographic factors, HCV alone was significantly associated with an increased risk for oral cavity cancer (HR = 1.90, 95%CI: 1.20-3.02). This positive association was highest among individuals in the 40-49-year age group (HR = 2.57, 95%CI: 1.21-5.46)[116].

Despite some potentials limitations, this study strongly suggests that, at least amongst Chinese ethnicity, HCV could represents a etiologic agent of OSCC and further perspective cohort studies are certainly warranted.

Notably, both positive and negative HCV-RNA strands were detected in oral cancer tissues[103], but further data are required for these preliminary observations to be confirmed.

In conclusion, HCV might be involved in oral carcinogenesis and more studies are needed to clarify this association.

OTHER DISEASES

Other disorders commonly causing oral lesions such as paraneoplastic pemphigus and pemphigus vulgaris and Behcet’s disease have been only anecdotally linked to HCV[117-125].

CONCLUSION

At least three of the most studied EHM of HCV infection, involve the oral region predominantly or exclusively. Convincing epidemiological evidence support the association between OLP and HCV. As HCV may replicate in the oral mucosa and attract virus-specific T lymphocytes, it may be implicated in OLP pathogenesis. Conversely, the epidemiologic and pathogenetic role of HCV in SjS development and the characteristics distinguishing classic SjS from HCV-related sialadenitis are still controversial. Emerging recent data highlight a possible link between OSCC and HCV and further studies are clearly warranted.

Footnotes

P- Reviewers: Gara N, Lin RT S- Editor: Wen LL L- Editor: A E- Editor: Ma S

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