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 of bacterial or viral origin, 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.
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.
Clinically, there is a rapid attachment loss of the gingival tissue alongside rampant bone destruction, either localized or through single or multiple quadrants of the mouth.
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.
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.
Genetic diseases affecting children, such as Leukocyte adhesion deficiency, Papillon Lefevre syndrome, Chediak Higashi syndrome, neutropenia, hypophosphatasia, agranulocytosis, and trisomy of 21 chromosomes, are also associated with the early development of aggressive periodontitis.
The manifestations of aggressive periodontitis always subsequently damage oral immune host defense, leading to premature tooth loss in younger individuals.
What Is the Pathogenesis of Herpes Virus in Aggressive Periodontal Disease?
Clinicians have researched and analyzed the occurrence of herpes viruses in aggressive types of periodontal disease using both qualitative and quantitative identification techniques. The standard hypothesis proposed is that co-infection through the herpes virus may be more prevalent because the development and progression of periodontal disease are in direct conjunction with attacking or invading the host of oral immune defense against certain opportunistic pathogenic bacteria that reside endogenously in the oral microbiota sub gingivally.
An increase in the local pro-inflammatory cytokines, the primary inflammatory mediators in this process, mainly breaks the homeostatic balance in a healthy periodontium between the existing microflora in the host.
Pathogenic organisms present in the subgingival microflora tend to infiltrate within such inflammatory conditions.
Pathogens such as P. gingivalis, T. forsythia, and Treponema spp. increase and help progress aggressive periodontitis.
Another major hypothesis explains the pathogenesis of infectious mechanisms by cytomegalovirus infection initiated during the formation of the tooth root; when this viral pathogen is reactivated during the pubertal phase of life, viral pathogen infiltration may be easier for the progression of aggressive periodontitis.
The above phenomenon lowers host immunity to the extent that periodontal tissue breakdown occurs faster, further facilitating the infiltration of viral pathogens like the herpes virus.
This malformation occurs during the development process of the periodontal attachment apparatus. Thus, this explains why 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 can also target 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 controls 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 indicates that herpes infections are a definite possibility within aggressive periodontitis. The saliva also contains many 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 salivary viral herpes levels and aggressive periodontitis. The treatment of aggressive periodontitis should include regular systemic antibiotic therapy. Dental researchers and clinicians recently analyzed the herpes virus infection models. It suggests that the bacterial or viral infiltration of lesions in aggressive periodontitis allows new considerations or protocols to be developed in preventing and treating the disease. This new model treatment or protocol, as recommended by periodontists, would be by treatment through antiviral drug therapy.
Conclusion:
Periodontology focuses on preventing tooth loss and reducing the risks of systemic diseases. Periodontal herpesviruses have a significant correlation with both tooth loss and systemic disorders. Research on the role of periodontal herpesviruses in non-oral disorders continues to be a significant area of study. The management and prevention of periodontal herpesviruses are fundamentally uncomplicated. Systemic and topical medication targeting herpesviruses can eliminate active infections, while proper patient self-care can prevent the infiltration of dormant herpes viruses into the periodontium. The dentist must educate 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 these periodontitis patients' dental and systemic prognosis.
