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The Importance of Viral Detection in Oral Fluids in Patients with Periodontal Disease

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The Importance of Viral Detection in Oral Fluids in Patients with Periodontal Disease Romanian Journal of Medical and Dental Education Vol. 9, No. 4, July - August 2020 THE IMPORTANCE OF VIRAL DETECTION IN ORAL FLUIDS IN PATIENTS WITH PERIODONTAL DISEASE. REVIEW. Alexandru Flondor1, Irina-Georgeta Sufaru2*, Maria-Alexandra Martu2, Ionut Luchian2, Liliana Pasarin2, Vasilica Toma3, Silvia Martu2 1DMD, PhD, Private Practice, Iasi, Romania 2University of Medicine and Pharmacy “Grigore T. Popa”, Faculty of Dental Medicine, Department of Periodontology, Iasi, Romania 3University of Medicine and Pharmacy “Grigore T. Popa”, Faculty of Dental Medicine, Department of Pediatric Dentistry, Iasi, Romania *Corresponding authors: Sufaru Irina-Georgeta. E-mail: [email protected] #All authors had equal contributions with the first author Abstract The direct involvement of herpesviruses in the evolution of periodontitis can change the concepts of pathogenesis and disease management. A double periodontal infection of herpesviruses and pathogenic bacteria tends to be associated with more severe periodontitis than a periodontal infection involving only bacteria. Classical techniques in viral diagnosis use cell culture or antigenemia. These diagnostic techniques have been largely replaced by DNA and / or RNA-based tests, which possess superior technical performance and cost advantages. False-negative and false-positive PCR results are an inherent concern. Poor design of the PCR test, without optimization or validation of the PCR methodology, may lead to inaccurate findings and incompatible with those of other studies. The concept of viral infections of the diseased periodontium may introduce a new level of understanding of the importance of preventing and controlling periodontal disease for medical purposes. Keywords: viruses, periodontal bacteria, saliva, crevicular fluid, PCR Introduction The etiopathogenesis of Gingivitis and periodontitis are periodontitis includes specific bacteria and infectious diseases that tend to be viruses [2], protective and destructive particularly severe in immune responses of the host [3], immunocompromised individuals [1]. modifiable and unchangeable Chronic gingivitis is relatively easy to environmental factors [4], and genetic and prevent and cure and virtually all types of epigenetic factors [5]. However, the periodontitis are controllable, but due to relative importance of different etiological delayed diagnosis of destructive determinants remains elusive due to the periodontal disease, therapy can be complex pathophysiology of periodontitis complex and expensive. Even after and divergent results in studies. Studies adequate periodontal treatment, the long- conducted since the mid-1990’s have term outcome may be unsatisfactory in identified a high prevalence and a large patients with poor adherence to an number of copies of cytomegalovirus, effective oral hygiene regimen or with Epstein-Barr virus and herpes simplex difficulty accessing professional virus type 1 in progressive periodontal periodontal care. The development of disease [6]. Evidence supporting a more effective therapies may require a periodontopathogenic role of better perspective on the aetiology of herpesviruses comes from association periodontal disease. studies and research based on 59 Romanian Journal of Medical and Dental Education Vol. 9, No. 4, July - August 2020 immunology, but the specific molecular viruses and varicella-zoster virus), B mechanisms by which herpesviruses can lymphocytes (Epstein-Barr virus, cause or exacerbate periodontitis have yet herpesvirus-8) or monocytes and T to be identified. The direct involvement of lymphocytes (cytomegalovirus and -6 and herpesviruses in the evolution of -7). periodontitis can change the concepts of Conversion of latent herpesvirus to pathogenesis and disease management. lytic replication may occur spontaneously or may be caused by environmental Herpesviruses stimuli, chemical agents, and events of Herpesvirus species comprise the physical and psychosocial stress, as found most widespread viral family in human in subjects under acute stress, astronauts in saliva and are important space flight, students before important periodontopathogenic agents. Eight academic exams, elite athletes in intensive species of herpesvirus, with distinct training and subjects with work-related biological and clinical characteristics, can fatigue. Reactivation of an oral herpesviral infect humans: herpes simplex virus-1 and infection can be estimated by an increase -2, varicella-zoster virus, Epstein-Barr in salivary herpesvirus counts or a virus, human cytomegalovirus, human significant increase in herpesvirus-specific herpesvirus-6, human herpesvirus-7 and salivary antibodies. Immunocompetent human herpesvirus 8 (Kaposi's sarcoma individuals usually experience the virus). Herpesviruses establish a persistent reactivation of herpesvirus that lasts only a infection throughout life, and some species few hours or days [9], which is probably of herpesvirus infect up to 90% of the too short a period of time to initiate or adult population [7]. exacerbate the clinical disease. However, The clinical outcome of a the release of herpesvirus virions into herpesvirus infection ranges from a saliva poses a risk for infection of subclinical or mild disease to encephalitis, individuals in intimate contact. pneumonia, and various cancers. In contrast, long-term Herpesviral infections of the oral cavity immunosuppressive conditions ⁄ diseases can lead to asymptomatic and and medications can lead to the unrecognized release of virions into saliva reactivation of oral herpesviruses that or diseases of the oral mucosa or continue for an extended period of time periodontium. One study looked at acute and may present a pathogenetic risk to the herpesviral infections in children's oral infected person. The immune system of cavities [8]. the elderly may not control a latent Herpesviruses have a cycle of varicella-zoster infection, resulting in biphasic infection that involves a lytic, outbreaks of shingles, or may not replicative (productive) phase and a latent, effectively protect against Epstein-Barr unproductive phase. The replication phase virus and cytomegalovirus reactivation involves the expression of viral regulatory [10]. Herpesvirus infection in such people and structural proteins and the formation can be characterized as chronically of infectious virion particles [7]. The reactivated instead of latent. ability to switch between replicative and The vast majority of systemically latent states ensures viral transmissibility healthy adults continuously release between individuals, as well as a herpesvirus DNA into saliva. Herpes permanent host infection. Following the simplex-1 virus DNA was detected in initial infection, herpesviruses saliva in amounts up to 2.0-2.8 · 106 ⁄ ml preferentially exist in a latent state in [11]. DNA copies of Epstein-Barr virus in sensory ganglion cells (herpes simplex saliva can reach levels of 108 ⁄ ml, 1.6 · 60 Romanian Journal of Medical and Dental Education Vol. 9, No. 4, July - August 2020 109 ⁄ ml [12], 7.1 · 105 ⁄ ml [13] and 2.2 · between salivary and subgingival levels of 106 to 0.5 lg of DNA [14]. Because the Epstein-Barr virus in one study [21], but salivary number of Epstein-Barr virus has not in another study [22]. decreased moderately only after high- Active periodontal volume oral rinsing, or after normal cytomegalovirus infection is closely linked swallowing every 2 minutes, a large to aggressive periodontitis [7]. amount of virus must enter the saliva Cytomegalovirus DNA was detected in the constantly [15]. However, the salivary saliva of 50% of periodontitis patients, but load of Epstein-Barr virus can vary over was not found in the saliva of gingivitis several months, which complicates the patients or total prosthesis wearers, classification of individuals as small, suggesting that salivary cytomegalovirus intermediate, or large viral release agents originates primarily from periodontitis [15]. Cytomegalovirus DNA was detected lesions [12]. in the saliva of 61% of immunocompetent Cytomegalovirus DNA from and immunocompromised subjects (65) infected breast milk also appeared in the and was able to reach a number of copies saliva of infants at 4 months of age, of saliva DNA of 4.2 · 104 ⁄ ml [12]. peaked at 4-10 months after birth, and Herpesvirus-6 and herpesvirus-7 can occur subsequently decreased or became in saliva, with prevalences exceeding 95% undetectable [23]. and in amounts of several million copies In short, a large part of salivary of DNA ⁄ ml [16]. Varicella-zoster virus herpeviruses are released from the sites of DNA is present at a low prevalence and in periodontal disease. Because periodontal amounts of <1.100 children ⁄ ml in the treatment can significantly reduce the saliva of both healthy people and people number of subgingival [24] and salivary infected with HIV [17]. herpesvirus DNA, establishing a healthy A double periodontal infection of periodontium can reduce the risk of herpesviruses and pathogenic bacteria transmitting herpesvirus and herpesvirus- gives rise to increased cytokine release and related diseases. The close relationship immune signalling disorder [18] and tends between some species of herpesvirus and to be associated with more severe periodontitis also supports the examination periodontitis than a periodontal infection of the potential use of the salivary involving only bacteria. herpesvirus number to indicate the risk of Herpes simplex-1 virus may periodontal disease. contribute to periodontitis in a subgroup of
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