What Viruses Play a Causal Role in Periodontal Diseases?

What viruses are involved in periodontal disease? EBV: Epstein-Barr virus; CMV: Cytomegalovirus; HHV: human herpes virus, HSV: Herpes simplex virus; VZV: Varicella-zoster virus.

Could your chronic or rapidly progressive periodontal disease involve viruses?  The short answer is yes, and we can affordably test you for them.  But more importantly, the presence of a viral component to your periodontal disease is more about what is going on with your immune system.  Understanding this leads to more in depth solutions if your clinician is being comprehensive.  The "why are the viruses there" answer is typically a susceptible host (compromised immune system).  It's our job as holistic periodontal providers to figure out why our patients are susceptible, and then work to correct the cause systemically. 

Viruses cannot be treated with 'topical treatments' alone, such as rinses or toothpaste, or professional treatments that do not involve removing ALL of the tartar/calculus lurking below the gum line (as with non visual root planing or laser surgery - no endoscope used). It's important to understand what is driving the chronic inflammation and bone and tissue loss, but its just as important to know how to help your patients achieve homeostasis (health/remission).  We help our patients work with other medical health care professionals to get to the root cause and restore the inflammatory response (chronic inflammation is very destructive, it is the true cause of periodontal disease).  Find out why you have chronic periodontitis and what can be done about it. 

Periodontal diseases can involve bacteria and/or viruses initiating
chronic inflammation and ensuing tissue and bone destruction.  Patients
with history of herpes simplex virus (HSV) or Epstein Barr virus (EBV)
are especially high risk for the presence of these putative pathogens. SimplyPerio saliva testing to either confirm or refute the presence of viruses in the risk factor assessment of active periodontitis can now be performed chairside. Topical rinsing to combat oral viruses may be helpful (grape seed extract or diluted bleach with water 1/20, but ideally the WHY needs to be addressed definitively.  Why is the host susceptible (attracting these pathogens) and how can we modify host response to achieve health and homeostasis. This is achieved not only by a thorough removal of all the toxic calculus in all pockets, but also by performing an in-depth analysis of host response (modifiable and genetic risk factors) so that we can treat the actual cause.  Learn more about our philosophy here.

Biology and Pathogenesis of Cytomegalovirus in Periodontal Disease:

Periodontol 2000. 2014 Feb;64(1):40-56. doi: 10.1111/j.1600-0757.2012.00448.x.
Biology and pathogenesis of cytomegalovirus in periodontal disease.
Contreras A, Botero JE, Slots J.
Abstract

Human periodontitis is associated with a wide range of bacteria and viruses and with complex innate and adaptive immune responses. Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacter actinomycetemcomitans, Treponema denticola, cytomegalovirus and other herpesviruses are major suspected pathogens of periodontitis, and a combined herpesvirus-bacterial periodontal infection can potentially explain major clinical features of the disease. Cytomegalovirus infects periodontal macrophages and T-cells and elicits a release of interleukin-1β and tumor necrosis factor-α. These proinflammatory cytokines play an important role in the host defense against the virus, but they also have the potential to induce alveolar bone resorption and loss of periodontal ligament. Gingival fibroblasts infected with cytomegalovirus also exhibit diminished collagen production and release of an increased level of matrix metalloproteinases.  This article reviews innate and adaptive immunity to cytomegalovirus and suggests that immune responses towards cytomegalovirus can play roles in controlling, as well as in exacerbating, destructive periodontal disease.

More research here:

https://pmc.ncbi.nlm.nih.gov/articles/PMC11551682/