Are Viral Infections Associated with Aggressive Periodontitis?
According to medical literature and research papers, the link between periodontal disease and systemic infections is quite evident. A broad spectrum of infections, whether bacterial or viral origins are directly related to periodontal disease. For example, HIV (human immunodeficiency virus), papillomaviruses, herpes virus and its types, CMV (cytomegalovirus), EBV (Epstein Barr virus), and human lymphotropic virus, etc.
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Aggressive periodontitis is characterized by aggressive inflammation of the gingival tissues and alveolar bone loss. Aggressive periodontitis is one of the main types of periodontal disease that is responsible for early tooth loss soon after the onset of the clinical features.
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There is clinically a rapid attachment loss of the gingival tissue alongside bone destruction that is rampant, either localized or through single or multiple quadrants of the mouth.
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Aggressive periodontitis mainly affects young people without any significant medical history and often shows a familial linkage. Though less frequent in occurrence than the chronic form of periodontitis, the presence of highly virulent microflora in this disease makes host immunity an easy target for invasion by specific bacteria or viral pathogens.
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Environmental factors or certain predisposing risk factors and triggers also play an equally important role in expressing aggressive clinical features specific to aggressive periodontitis, such as smoking, poor oral hygiene, alcoholism, subgingival deposits, psychological stress, and immune or systemic issues of an individual.
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Genetic diseases affecting children like Leukocyte adhesion deficiency, Papillon Lefevre syndrome, Chediak Higashi syndrome, neutropenia, hypophosphatasia, agranulocytosis, trisomy of 21 chromosomes, etc., are also associated with the early development of aggressive periodontitis.
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The manifestations of aggressive periodontitis always subsequently result in the damage of oral immune host defense, leading to premature loss of teeth in younger individuals.
What Is the Pathogenesis of Herpes Virus in Aggressive Periodontal Disease?
The occurrence of herpes viruses in aggressive types of periodontal disease has been researched and analyzed by clinicians through both qualitative and quantitative identification techniques.
The standard hypothesis proposed is that the co-infection through the herpes virus may be more prevalent because the development and progression of periodontal disease are in direct conjunction to attack or invade the host of oral immune defense against certain opportunistic pathogenic bacteria that reside endogenous in the oral microbiota sub gingivally.
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An increase in the local pro-inflammatory cytokines that are the primary inflammatory mediators in this process mainly breaks the homeostatic balance that normally exists in a healthy periodontium between the existing microflora in the host.
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Pathogenic organisms present in the subgingival microflora tend to infiltrate within such inflammatory conditions.
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Pathogens such as P. gingivalis, T. forsythia, and Treponema spp. eventually increase and help in the progression of aggressive periodontitis.
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Another major hypothesis explains the pathogenesis of infectious mechanisms by cytomegalovirus infection initiated during the formation of the tooth root; when there is a reactivation of this viral pathogen during the pubertal phase of life, then the viral pathogen infiltration may be easier for the progression of aggressive periodontitis.
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The above phenomenon lowers the host immunity to the extent that periodontal tissue breakdown occurs faster and further makes space for the infiltration by viral pathogens like the herpes virus.
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This malformation occurs during the development process of the periodontal attachment apparatus. Thus, this gives an explanation of why the patients suffering from aggressive periodontitis with herpes or other viral infections, in spite of reporting minimal tooth plaque, still tend to suffer from lowered immunity and viral pathogenesis.
What Is the Latest Treatment Plan for Herpes Virus Infection?
Herpes viruses are also capable of targeting not just immune cells but can target and colonize upon the host's immune functions. Other similar viral pathogenic potential is for the cytomegalovirus that attacks periodontal monocytes and macrophages, T lymphocytes, and the EBV (Epstein Barr virus) that infects B lymphocytes of the periodontium. The host immune response attempts to control both bacterial and viral invasion within periodontal pockets. The primary reasons why host immunity breaks down in this form of periodontal disease are the role of pre-existing malformations within the host periodontium and the defense activity of mainly inflammatory mediators like cytokines and chemokines. The discovery by dental researchers and microbiologists suggests that an abundant quantity of herpes viruses in any periodontal lesion clearly indicates that herpes infections are a definite possibility within aggressive periodontitis. The saliva also contains a high proportion of herpes viruses (like EBV, cytomegalovirus, herpes virus six, and herpesvirus 7).
Therefore, the dentist always recommends conventional periodontal treatment to reduce the number of viral genomic copies in the patient's saliva. Research also suggests that periodontal pocket infection would be a significant causative factor for increased herpes virus counts in saliva. The dentist or periodontist should educate the patient regarding the needs and potentials of conventional periodontal therapy in treating or reducing both salivary viral herpes levels as well as aggressive periodontitis. The treatment of aggressive periodontitis should definitely include regular systemic antibiotic therapy. The herpes virus infection models were analyzed by dental researchers and clinicians recently. It suggests that the bacterial or viral infiltration of lesions in aggressive periodontitis allows scope for new considerations or protocols to be developed in the prevention and treatment of the disease. This new model treatment or protocol, as recommended by periodontists, would be by treatment through antiviral drug therapy.
Conclusion: The dentist needs to educate the patients suffering from aggressive periodontitis on the additional risk of viral infection with herpes commonly associated. Timely management by the dentist and regular conventional periodontal therapy alongside systemic antibiotic treatment will improve the dental and systemic prognosis of these periodontitis patients.
