Article

Detection of hepatitis C virus RNA from gingival crevicular fluid and its relation to virus presence in saliva

Department of Infectious Diseases, University Medical Centre, Ljubljana, Slovenia.
Journal of Periodontology (Impact Factor: 2.57). 02/2001; 72(1):11-6. DOI: 10.1902/jop.2001.72.1.11
Source: PubMed

ABSTRACT To search for a possible source of hepatitis C virus (HCV) in saliva, the presence and shedding patterns of HCV in gingival crevicular fluid (GCF) and saliva of HCV viremic patients were assessed based on clinical, biochemical, histological, virological, and oral health parameters.
Saliva and GCF samples of 50 HCV viremic patients were collected to detect HCV RNA by a modified commercial polymerase chain reaction (PCR) assay. Clinical oral examination was performed and periodontal status at the collection sites was monitored. The results were correlated to specified parameters.
HCV RNA was detected in 59% (29/49) of the GCF specimens and in 35% (17/48) of the saliva specimens. In saliva specimens, HCV RNA was detected only in cases which also had detectable HCV RNA in the GCF samples (P=0.00002) and was significantly related to the presence of blood in saliva (P=0.03). Higher, but not significant, values of oral clinical parameters at the sites of fluid collection were found in GCF specimens harboring HCV RNA. In GCF specimens with no blood detected, HCV RNA was more often present in cases with higher plasma viral load (P=0.05).
The results suggest that besides blood, the other most probable source of HCV in saliva is GCF. Unknown endogenous HCV inhibitory mechanisms in the oral cavity may explain the discrepancies in HCV appearance between saliva and GCF. The results provide a biologic basis for further investigation of the role of HCV in the pathogenesis of periodontal disease.

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    • "However, HCV RNA has been measured in the saliva of infected individuals independent of mucosal lesions and periodontal disease (Liou et al. 1992, Fabris et al. 1999, Hermida et al. 2002, Lins et al. 2005). Additionally, HCV could enter the saliva via peripheral blood mononuclear cells (PBMCs) (Roy et al. 1998, Fabris et al. 1999, Maticic et al. 2001); however, the presence of HCV RNA in PBMCs and saliva have not been closely correlated (Young et al. 1993). The detection of HCV RNA in saliva and the existence of a correlation between the viral load in saliva and other compartments have been demonstrated in previous studies (Mariette et al. 1995, Hermida et al. 2002, Eirea et al. 2005, Lins et al. 2005, Wang et al. 2006, Farias et al. 2010). "
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    • "increased risk of HCV transmission to exposed individuals [Chen et al., 1995; Piazza et al., 1995]. Some studies found an association between HCV infection and sialadenitis [Haddad et al., 1992; Jorgensen et al., 1996]; however, the correlation between periodontal disease and HCV in saliva is not well established [Maticic et al., 2001]. A number of epidemiological studies report an association between HCV in the saliva of patients with oral lichen planus [Bagan et al., 1998; Nagao et al., 1995], although this is not always the case [Tucker and Coulson, 1999]. "
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    ABSTRACT: Tissue destruction associated with the periodontal disease progression is caused by a cascade of host and microbial factors and proteolytic enzymes. Aberrant laminin-332 (Ln-332), human beta defensin (hBD), and matrix metalloproteinase (MMP) functions have been found in oral inflammatory diseases. The null-allele mouse model appears as the next step in oral disease research. The MMP-8 knock-out mouse model allowed us to clarify the involvement of MMP-8 in vivo in oral and related inflammatory diseases where MMP-8 is suggested to play a key role in tissue destruction. The cleaved Ln-332 γ2-chain species has been implicated in the apical migration of sulcular epithelial cells during the formation of periodontal pockets. We demonstrated that increased Ln-332 fragment levels in gingival crevicular fluid (GCF) are strongly associated with the severity of inflammation in periodontitis. Porphyromonas gingivalis trypsin-like proteinase can cleave an intact Ln-332 γ2-chain into smaller fragments and eventually promote the formation of periodontal pockets. hBDs are components of an innate mucosal defense against pathogenic microbes. Our results suggest that P. gingivalis trypsin-like proteinase can degrade hBD and thus reduce the innate immune response. Elevated levels and the increased activity of MMPs have been detected in several pathological tissue-destructive conditions where MMPs are shown to cleave extracellular matrix (ECM) and basement membrane (BM) molecules and to facilitate tissue destruction. Elevated levels of MMP-8 have been reported in many inflammatory diseases. In periodontitis, MMP-8 levels in gingival crevicular fluid (GCF) and in peri-implant sulcular fluid (PISF) are elevated at sites of active inflammation, and the increased levels of MMP-8 are mainly responsible for collagenase activity, which leads to tissue destruction. MMP-25, expressed by neutrophils, is involved in inflammatory diseases and in ECM turnover. MMP-26 can degrade ECM components and serve as an activator of other MMP enzymes. We further confirmed that increased levels and activation of MMP-8, -25, and -26 in GCF, PISF, and inflamed gingival tissue are associated with the severity of periodontal/peri-implant inflammation. We evaluated the role of MMP-8 in P. gingivalis-induced periodontitis by comparing MMP-8 knock-out (MMP8-/-) and wild-type mice. Surprisingly, MMP-8 significantly attenuated P. gingivalis-induced site-specific alveolar bone loss. We also evaluated systemic changes in serum immunoglobulin and lipoprotein profiles among these mouse groups. P. gingivalis infection increased HDL/VLDL particle size in the MMP-8-/- mice, which is an indicator of lipoprotein responses during systemic inflammation. Serum total LPS and IgG antibody levels were enhanced in both mice groups. P. gingivalis-induced periodontitis, especially in MMP-8-/- mice, is associated with severe alveolar bone loss and with systemic inflammatory and lipoprotein changes that are likely to be involved in early atherosclerosis. Parodontiitti ja peri-implantiitti ovat kroonisia tulehdussairauksia hampaita ja keinojuuria eli implantteja ympäröivissä kiinnityskudoksissa. Bakteerien aineenvaihduntatuotteet, entsyymit ja toksiinit, sekä isännän oma puolustusvaste vieraille antigeeneille johtavat parodontiitin ja peri-implantiitin taudinkuville tyypilliseen kova- ja pehmytkudosten tuhoutumiseen ja lopulta hampaiden ja implanttien löystymiseen ja irtoamiseen. Tutkimuksen tavoitteina oli selvittää tiettyjen entsyymien ja proteiinien esiintyminen, ilmentyminen ja aktiivisuus hampaiden kiinnityskudosten tulehduksen isäntävasteessa, tarkentaa MMP-8-entsyymin todellisia vaikutuksia elävässä elimistössä poistogeeni (knock-out) -hiirimallilla sekä lisäksi syventää tietämystä elimistön oman puolustusvasteen roolista kroonisessa tulehduksessa. Hypoteesina oli edellä mainittujen molekyylien mahdollinen aktiivisuus parodontiittissa ja peri-implantiitissa sekä aktiivisuuden merkitys parodontiitin ja peri-implantiitin diagnostiikassa, isännän omassa puolustuksessa ja taudinkuvalle tyypillisessä kiinnityskudostuhossa. Tutkittujen molekyylien aktiivisuus ja ilmentyminen tulehtuneessa ientasku- ja peri-implanttinesteessä tai ienkudoksessa voimistuu tulehduksen vakavuuden myötä. Näiden molekyylien ja entsyymien kohonneet tasot ja aktiivisuuden nousu kuvastavat parodontaali- ja peri-implantti-infektioiden vakavuutta ja osallistuvat tulehduksen syntyyn ja etenemiseen toimien samalla tulehduksen biomarkkereina. MMP-8 toimii osittain suojaavana molekyylinä P. gingivaliksen aiheuttamassa paikallisessa ja systeemisessä tulehdusvasteessa. Totaalinen MMP-8 puutos johtaa lisääntyneeseen alveoliluukatoon sekä seerumin lipoproteiinien muutokseen ateroskleroottisempaan suuntaan. Parodontiitin hoidossa tulisikin keskittyä patologisesti kohonneiden MMP-8 tasojen alentamiseen lähelle normaalia, fysiologista tasoa sen sijaan että MMP-8 tuotantoa ja toimintaa pyritään kokonaan estämään.
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