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 Table of Contents  
Year : 2015  |  Volume : 2  |  Issue : 1  |  Page : 37-41

The roles of viruses in periodontal diseases

1 Department of Periodontics, University of Benin, Benin City, Nigeria
2 Department of Periodontics, University of Benin Teaching Hospital, Benin City, Nigeria

Date of Web Publication8-Apr-2015

Correspondence Address:
Dr. C C Azodo
Department of Periodontics, University of Benin, Benin City
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2348-2915.154650

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The roles of bacteria in the etiopathogenesis of periodontal disease are well-understand, but that of the virus found in the periodontal environment are poorly understood. The aim of this literature review was to report the roles of viruses in periodontal diseases. The roles of viruses in periodontal diseases were categorized into the role in disease etiology, role in the pathogenesis of periodontal diseases, role in diseases progression and role in response to treatment. Clearer understanding of roles of viruses in periodontal diseases will facilitate the provision of effective periodontal disease prevention and treatment.

Keywords: Pathogenesis, periodontal disease, virus

How to cite this article:
Azodo C C, Erhabor P. The roles of viruses in periodontal diseases. J Dent Res Rev 2015;2:37-41

How to cite this URL:
Azodo C C, Erhabor P. The roles of viruses in periodontal diseases. J Dent Res Rev [serial online] 2015 [cited 2023 Apr 2];2:37-41. Available from: https://www.jdrr.org/text.asp?2015/2/1/37/154650

  Introduction Top

Periodontal diseases are those diseases that affect one or more of the periodontal tissues: Gingiva, periodontal ligament, cementum and alveolar bone. [1] Different classifications of periodontal diseases have been used over the years and have been replaced as the understanding of the etiology and pathology of the diseases of the periodontium improved with increased scientific knowledge. The most recent classification is based on the 1999 International Workshop for the Classification of the Periodontal Diseases organized by the American Academy of Periodontology. [2],[3] Here viral diseases of the periodontium were placed under non-plaque induced gingival lesions, and they include herpetic gingivostomatitis, varicella zoster and others.

Viruses are one of the smallest forms of microorganism (10-100 nm) which can only multiply inside living cells. [4] It consist of the nucleocapsid, which may be "naked," or "enveloped" within a lipoprotein sheath derived from the host cell membrane.

  Classification of Viruses Top

Viruses are classified according to nucleic acid composition: Deoxyribonucleic acid (DNA) or ribonucleic acid (RNA). Some examples of DNA viruses are: Herpes viruses (herpes simplex virus [HSV], Varicella-zoster virus [VZV], Epstein-Barr virus [EBV], Cytomegalovirus [CMV], human herpes virus 6, Pox viruses, Papillomavirus, Hepatitis B virus and Some examples of RNA viruses are: Orthomyxoviruses, Influenza virus, Paramyxoviruses, Parainfluenza, Mumps, Measles, Toga viruses, Rubella, Retroviruses, Human immunodeficiency, viruses, Rhabdoviruses, Rabies, double-stranded Reo viruses, Rotavirus, Picornaviruses, Rhinovirus, Enterovirus, Coxsackie virus, Echovirus, Polio virus.

  Pathogenesis of Viral Diseases Top

Viruses usually gain entry into the host through different routes which include: (a) Inoculation (via the skin and mucosa) as in needle stick injury, bites or accidental abrasions (b) inhalation (via the respiratory tract) as in aerosol or droplet (c) ingestion (via the gastrointestinal tract) as in the feco-oral route and (d) the genitourinary tract as in sexual activity.

Once, the virus enters the host cell through direct local spread on epithelial and subepithelial surfaces, lymphatic spread, vascular spread, and central nervous system and peripheral nerve spread, it can interact with the host cell in two main ways namely permissive and nonpermissive mode.

  • Permissive infection: Here, there is a synthesis of viral components, their assembly and release with a consequent death of the host cell
  • Nonpermissive infection: Here, the infection can result in cell transformation often with the integration of viral DNA into the host genome. Here, there is viral replication within the cell but the cell remains alive. Examples are hepatitis B viruses, herpes viruses and retroviruses infection. [5]

  The Roles of Viruses in Periodontal Diseases Top

Role in disease etiology

Viruses can cause severe acute oral and orofacial disease, produce oral signs of systemic infection and be transmitted to patients and dental staff. Therefore, the role of viruses in the etiology of periodontal diseases can be divided into direct and indirect roles depending on whether they cause periodontal disease locally or as a result of the presence of a systemic infection.

Direct role in periodontal disease etiology

Herpes simplex virus infection

Herpes simplex virus, which are of two types: HSV-1 and HSV-2 are known to commonly cause skin and mucous membranes infections.

Herpes simplex virus-1 infections occur in the oral cavity while HSV-2 infections occur in the genital area. However, they can occur in either area and at other sites in the body. These viruses can be carried in body fluids or in fluid from herpes lesions. For an infection to occur, the viruses must gain entry into the body of the uninfected persons through their skin or mucous membrane in the intraoral or genital area. Once the virus has contact with the cells of the mucous membranes or skin tissue, it tries to replicate in the cell nuclei. This can result in symptoms following multiplication and destruction of the vulnerable cells of the skin and mucus membrane in previously uninfected individuals with inflammation and appearance of vesicles. After this initial infection, the virus is transported through the nerve cell to their sensory dorsal root ganglion where it becomes latent for a period of time. Autoinoculation, which is process by which infected individuals infect other parts of their own bodies, may occur. However, this is uncommon because of the development of protective antibodies against this problem among affected individuals.

The primary oral infection causes symptoms, which can be very painful, particularly in young children. This primary lesion is called primary herpetic gingivostomatitis, which is characterized by the formation of vesicles on the gingival, lips, tongue and buccal mucosa. The rupture of the vesicles results in painful erosion and ulceration with yellowish membrane development before healing, but disappears within 3-14 days. There is also associated increased salivation and bad breath. Rarely, chills, myalgia, dysphagia, or hearing loss may occur. [6]

Recurrences known commonly as herpes labialis, which usually affects the lips or the adjacent skin, are usually milder than the primary infections. It is usually caused by the reactivation of the latent virus. Following the primary HSV infection, virions travel from the initial site of infection on the skin or mucosa to the sensory dorsal root ganglion, where latency is established. When the dormant virus in the ganglion is activated, it begins to multiply again and moves down the trigeminal nerve usually to the site of initial inoculation and infect the epithelial cells causing a recurrent infection. [7] This is considered as ganglion trigger theory. The other, the skin trigger theory proposed by Hill and Blyth, holds that virus is continuously shed from neuronal endings and lesions develop when the susceptibility of the skin is sufficiently permissive for the development of a clinically apparent infection. [8] This showcases the unresolved nature of proposed theories concerning the mechanism of development of recurrent HSV infections. [8]

Reactivation of latent virus can be triggered by physical injury, trauma, surgery, sunlight, wind, cold, fever, immune suppression, upper respiratory tract infection, emotional stress and physiological event like menstruation. Trigger of latent virus within about 3 days of intense dental work like root canal treatment or tooth extraction have been reported. [9],[10]

Varicella zoster virus

The vesicular stomatitis virus or human herpes virus-3 (HHV-3) cause Chicken pox, which is the primary infection of VZV and this is followed by latency. Recurrence can occur as herpes zoster often after many decades. The virus is presumed to spread through air droplets or direct contact with an active lesion. The periodontal lesion is indistinguishable from HSV except that the lesion of chicken pox tends to be relatively painless. Herpes zoster is characterized by pain and rash in one dermatome. Pain that persists long after the rash has healed is recognized as postherpetic neuralgia. [11]

Kaposi sarcoma herpes virus

This is also known as HHV8 and has been identified in all forms of Kaposi's sarcoma lesions. This virus is believed to have a significant role in the induction and/or maintenance of Kaposi's sarcoma. Different clinical patterns of Kaposi's sarcoma have been described: The classic, endemic, iatrogenic immunodeficiency-associated as well as Acquired Immune Deficiency Syndrome (AIDS)-related Kaposi sarcoma. Oral lesions are frequently seen in the immunodeficiency state than in other forms of Kaposi sarcoma. Kaposi's sarcoma has been described in most oral regions, although the palate, gingiva, and tongue seem to be the most commonly affected sites. [12]

Cytomegalovirus infection

Cytomegalovirus or HHV-5 is a herpes virus that infects most persons at some time during their lives. It is similar to other HHV that is, after infection, latency is established and reactivation is possible after conditions favorable to the virus. This infection is often subclinical and usually occurs in young children but may also be seen in adolescents and adult. It is common in the developing world especially among the low socioeconomic group. In infants, the virus is contracted through the placenta, during delivery or during breast feeding. Transmission occurs during adolescence during sexual activity. Transmission has also been documented during blood transfusion and organ transplantation. [13] Patients with immune defects are liable to severe and/or protracted infections, or the virus reactivation. [14]

  • Infection in normal children or adults is usually asymptomatic, but the virus thereafter remains latent in the body. Symptomatic CMV infection in otherwise apparently healthy children and adults causes the CMV mononucleosis syndrome of headache, back and abdominal pain, sore throat, fever and atypical lymphocytosis
  • Transplacental infection may result in abortion, learning disability or other defects, and the affected child excretes CMV in the urine for months or years after birth and is a major reservoir of the virus
  • In immunocompromised patients, such as those with renal transplants and patients with human immunodeficiency virus (HIV)/AIDS, CMV acts as an opportunistic infection and may cause serious disease involving the lungs, liver, gastrointestinal tract, central nervous system and eyes. Chronic oral mucosal ulcerations have been documented especially in patients with HIV and may demonstrate co-infection with other viruses. [15]

Indirect role in periodontal disease etiology

Human immunodeficiency virus: The most frequent routes of transmission of HIV are sexual contact, parenteral exposure to blood or mother to child transmission. The primary target of HIV is CD4 + helper T cells. The HIV become incorporated into the DNA of the lymphocyte and become present for the life of the cell. It may remain latent for a period of time but soon becomes active and cause cell death. A subsequent decrease in the number of T helper cell number occurs with a resultant loss in immune function. It is this reduction in immune function that predisposes the individual to a number of opportunistic infection including periodontal diseases and some of the viral infection discussed above. The EC Clearinghouse on Oral Problems Related to HIV Infection and WHO Collaborating Centre on Oral Manifestations of the HIV classified periodontal diseases as lesions strongly associated with HIV infection. [16]

Periodontal diseases are common among HIV-infected patients, and they are characterized by gingival bleeding, bad breath, pain/discomfort, mobile teeth, and sometimes sores. Its reported prevalence ranges widely, between 0% and 50%. If left untreated, HIV-associated periodontal disease may progress to life-threatening infections, such as Ludwig's angina and cancrum oris. Four forms of HIV-associated periodontal disease have been described: Linear gingival erythema, necrotizing ulcerative gingivitis (NUG), necrotizing ulcerative periodontitis (NUP), and necrotizing stomatitis.

  • Linear gingival erythema is characterized by the presence of a 2-3 mm red band along the marginal gingiva, associated with diffuse erythema on the attached gingiva and oral mucosa. The degree of erythema is disproportionately intense compared with the amount of plaque present on the teeth
  • NUG is more common in adults than in children. It is characterized by the presence of ulceration, sloughing, and necrosis of one or more interdental papillae, accompanied by pain, bleeding, and mouth odor
  • NUP is characterized by the extensive and rapid loss of soft tissue and teeth
  • Necrotizing stomatitis is thought to be a consequence of severe, untreated NUP. It is characterized by acute and painful ulceronecrotic lesions on the oral mucosa that expose underlying alveolar bone.

Role in pathogenesis of periodontal diseases

Viral infection contributes to the development of various forms of periodontal diseases including severe chronic periodontitis, localized and generalized aggressive periodontitis, HIV-associated periodontitis and acute NUG. [17] The possible role of viruses in periodontal diseases is suggested by the recovery of a patient from a chronic and highly treatment refractory periodontal condition upon antiviral treatment. [18] Moreover, these viruses are found significantly more frequently in samples taken from disease active pockets, and gingival crevicular fluid compared to healthy pockets. [19],[20] Whereas several viruses are known to be involved in oral diseases, Herpes virus, as well as the HIV play a more relevant role in periodontal diseases. [21]

Herpes virus infections generally involve three phases, which include (1) a mild or asymptomatic primary phase, followed by (2) an asymptomatic latent phase. Sporadically, the asymptomatic latent phase is interrupted by periods of activation, where viral replication and clinical disease may become manifest. The reactivation of the herpes virus is triggered by a number of immunosuppressing factors. As these viruses are contact transmitted, either by means of virus production in the skin accompanied by vesicles or viral presence in sputum and saliva. In addition to the traditional clinical manifestations of EBV and CMV and HSV described above, they have been associated with periodontal diseases. [22],[23]

The pattern of herpes viral infection may explain several hallmarks of periodontal diseases such as: (a) Episodic progressive nature of periodontal disease due to transient local immunosuppression depending on active or latent viral infection); (b) localized pattern of tissue destruction (due to viral tissue tropism); (c) some individuals carry periodontopathogenic bacteria and still maintain periodontal health due to absence of viral infection.

These viruses play a fundamental role in the pathogenesis of periodontal diseases by a number of mechanisms operating alone or in combinations namely:

  • Direct cytopathic effect on inflammatory cells such as polymorphonuclear, leukocytes, lymphocytes, macrophages, and other cells such as fibroblasts, endothelial cells and even bone cells. Herpes virus-induced cytopathic effects will hamper tissue turnover and repair as the involved are the main constituents of inflamed periodontal tissue [24]
  • Cytokines and chemokines release: Their release from inflammatory and noninflammatory host cells are mediated by viruses. [17] Cytokine are cell products of different kinds of cells such as leukocytes, keratinocytes, resident mesenchymal cells, dendritic cells and endothelial cells. Cytokines stimulate inflammatory cells, which if not contained results in destruction of the connective tissue alveolar bone. Some of them can stimulate one or more steps of bone resorption by recruiting, differentiating or fusing of precursor cells to form osteoclasts or to enhance osteoclast survival. Chemokines, which are chemotactic cytokines attracting leukocytes, contribute to the process of destruction of mineral tissue during bone resorption because macrophages release matrix metalloproteinases (MMPs). MMPs are structurally related endopeptidases usually divided into several subclasses according to their substrate specificities and physical structure: Interstitial collagenases, gelatinizes. They are involved in the degradation process of different extracellular molecules such as collagen, elastin, proteoglycans, and laminins. MMPs are considered to be of great clinical importance in the pathogenesis of periodontal disease due to their ability to activate latent forms of effector proteins such as antimicrobial peptides, chemokines and cytokines [25]
  • Interference with the immune system of the host: EBV infects periodontal B-lymphocytes, and CMV infects periodontal monocytes/macrophages and T-lymphocytes in periodontitis lesions. [26] The down regulations of these cells involved in the periodontal defense may lead to bacterial superinfection resulting in increased virulence of resident bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, Campylobacter rectus, Treponema denticola and Aggregatibacter actinomycetemcomitans.[27] Human CMV (HCMV) and EBV have been reported frequently in aggressive periodontitis sites, in chronic periodontal disease as well as periodontal disease associated with systemic diseases [19]
  • Promotion of bacteria colonization: The promotion of subgingival attachment and colonization of periodontopathic bacteria occurs in gingival herpes virus infection, which is an illustration of enhanced bacterial adherence to virus-infected cells that exists in some other viral infections. [28] This enhanced presence of periodontopathic bacteria results in a more severe periodontitis. The expressed viral proteins on eukaryotic cell membranes, which act as bacterial receptors and help generate new bacterial binding sites is an enhanced bacterial adhesion mechanism. [24] Exposed basement membrane and surface of regenerating cells resulting from the loss of virus-damaged epithelial cells are known to provide new sites for bacterial binding [27]
  • Herpes virus - Bacteria Synergy: Herpes viruses interaction with specific bacterial species are considered as an important pathogenetic feature of periodontitis. [29] Initially, dental plaque bacteria cause gingival inflammation, which facilitates the entry of herpes virus-infected inflammatory cells into the periodontium. The subsequent reactivation of the herpes virus in the gingival tissue spontaneous or as a result of various types of the host immune defense impairment may then aggravate the periodontal disease. These host immune defense impairment factors such as including HIV infection, pregnancy, hormonal changes, and psychosocial and physical stress are recognized risk indicators of periodontal diseases. [30] Bacterial activity, for example, bacterial enzymes or other inflammation-inducing products, on the other hand, can also activate periodontal herpes viruses, which are considered as the vicious circle concept. Herpes viral-bacterial interactions may help explain the destructive periodontal disease burst-like episodes characteristics. Alteration of prolonged latency periods with periods of activation of herpes viral infections may be partly responsible for the burst-like episodes in the periodontitis progression. Absence of herpes viral infection or its reactivation helps to explain why some individuals carry periodontopathic bacteria and still maintain periodontal health or minimal disease while frequent reactivation of periodontal herpes viruses help account for the rapid periodontal breakdown in some patients even in the presence of relatively little dental plaque. Tissue tropism of herpes viral infections is a contributory explanation for the localized pattern of tissue destruction in periodontitis
  • Immunopathologic responses: HCMV can induce cell-mediated immunosuppression by interfering with cytotoxic T-lymphocyte recognition through the down-regulating cell surface expression of major histocompatibility complex class I molecules. It interferes with the induction of major histocompatibility class II antigens and inhibits natural killer cell activity. HCMV may lead to global impairment of cell-mediated immunity by suppressing antigen-specific cytotoxic T-lymphocyte functions, which now results in an increase in CD8 + suppressor cells and a decrease in circulating CD4 + cells
  • EBV may induce proliferation of cytotoxic T lymphocytes whose the main purpose are recognition and destruction of virally infected cells. However, various aspects of the periodontal immune response may be hampered secondarily by EBV. [24] Together, these mechanisms probably contribute to the pathogenesis of periodontitis.

Role in diseases progression

Viruses, as evident by most of the herpes viruses, go into latency after the primary infection and reactivation is possible in the condition favorable to the virus. Immunocompromised patients tend to experience more severe symptoms than the immunocompetent individuals. HIV also goes into latency after the initial infection to recur later. They predispose the individual to a number of opportunistic infections that progress faster and present more severe symptoms than those occurring in immunocompetent individuals.

Role in response to treatment

Although most periodontal diseases of viral origin resolve spontaneously, antiviral agents such as acyclovir, ganciclovir, valacyclovir and famciclovir accelerate the healing of the lesion and reduce the duration of pain. However, these drugs must be begun early enough in treatment to be effective. They may be given by the intravenous route in the immunocompromised patients and have been useful in the resolution of the lesions in a number of cases.

Human immunodeficiency virus responds to a number of highly active antiretroviral agents. These do not result in total eradication of the virus but greatly reduce their multiplication thus helping in the clinical improvement of the patient. Kaposi Sarcoma, being a vascular neoplasm respond to the chemotherapeutic agent especially vinblastine in the control of the lesion.

  Conclusion Top

The role of viruses in periodontal diseases cannot be over emphasized as they have shown to modify the disease condition especially in the immunocompromised patients; the good news is that they are responsive to antiviral agents especially when instituted early in the course of the disease condition.

  References Top

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