Viruses are an extremely important component of periodontal disease, both in its initiation and in the ongoing promotion of the attack process. Viruses that initially stem from the mouth also may have much wider systemic impacts dental supplies. Several years ago, Jorgen Slots, DDS, PhD, a professor of dentistry at the University of Southern California, reported that herpesviruses [both Epstein-Barr virus type 1 (EBV-1) and human cytomegalovirus (HCMV)] are some of the unrecognized major viruses implicated1 in periodontal attack. Unfortunately, when one transitions from the study of bacteria to consideration of viruses, most dentists cringe, since the profession has the least training in comprehending that submicroscopic world. Herpesviruses are a leading cause of human viral diseases. There are 9 herpesvirus types known to infect humans: herpes simplex viruses (HSV-1 and HSV-2), varicella-zoster virus (chicken pox and shingles), Epstein-Barr virus (EBV or HHV-4), human cytomegalovirus (HCMV or HHV-5), human herpesvirus (HHV-6A, HHV-6B, and HHV-7), and Kaposi’s sarcoma-associated herpesvirus (KSHV)2. Ruth F. Itzhaki, PhD, MSc, MA3, demonstrated that the herpes simplex virus type 1 (HSV1), the same virus that causes cold sores in the mouth, is present in the elderly human brain. Once HSV1 infects the epithelial cells of the mucous membranes of the face, it secondarily infects sensory nerve terminals. After it enters the neuron, HSV1 moves to the neuronal cell body in the trigeminal ganglion, located at the base of the skull adjacent to the brain stem. HSV1 remains in the ganglion in a latent form until reactivation, when the newly synthesized virus is retrograde transported more peripherally4, eventually leading to visible outbreaks such as on the lip. In older subjects, this highly prevalent virus reactivates and enters the brain by way of the peripheral nervous system or the olfactory route5. Though it becomes latent in the brain, it periodically reactivates in association with stressors such as systemic infection and immunosuppression dental lab equipment. Spirochetes, HSV1, Beta Amyloid, and Systemic Diseases Pathogen-induced inflammation and central nervous system accumulation of beta amyloid (Aβ) (Figure 1) damages the blood-brain barrier, which contributes to the pathophysiology of Alzheimer’s disease (AD)6. Data for both Chlamydophila pneumoniae and spirochetes7,8 shows a high prevalence of these pathogens in AD brains only, suggesting that secondary C pneumoniae and/or spirochete infection of the brain may occur after preliminary HSV1 and other co-factors have already initiated AD pathogenesis9. Since spirochetes can invade all tissues of the body via circulatory pathways10, they may be the instigators of the inflammation that damages the lining of blood vessels and possibly deteriorates the blood brain barrier11. Spirochetes also can take the trigeminal nerve pathway to the brain. Thus, the activation of the already present latent HSV1 by spirochetes in the brain could represent the final step in a series of infections leading to full blown Alzheimer’s disease. Amyloid plaques, the hallmark of AD, contain fibrillar Aβ (Figure 2). HSV1 has been implicated as a risk factor for AD and found to co-localize within Aβ plaques. Aβ peptides represent anti-infective peptides that protect against neurotropic virus infections such as HSV1 (Figure 3). The Aβ peptide may protect against latent herpes viruses and other infections. This antimicrobial property may explain why Aβ plaque formation plays a pathogenic role in the progression of the sporadic form of AD because it is reacting to an infection12,13. Very recent research has shown that Aβ plaque in AD is an active biofilm of viable Borrelia spirochetes in Alzheimer’s disease patients. Alan MacDonald, MD, presented compelling evidence from brain tissue harvested from deceased Alzheimer’s patients. In his 37-minute video14, Borrelia Chronic Brain Infections and Development of Alzheimer’s Disease, MacDonald used specific DNA marker probes to ascertain the presence of Borrelia burgdorferi spirochetes (implicated in Lyme disease). According to MacDonald, 100% of the samples tested demonstrated that active biofilms of various forms of Borrelia were enveloped within Aβ. For the first time, MacDonald demonstrated the spore-like role of granular forms of borrelia as viable, virulent pathogens, distinct from the easily recognized spiral corkscrew shaped forms. He identified round body forms of spirochetes in the evolution of AD. All these forms live within active biofilm communities previously characterized as undefined, dead, brown-appearing lesions called Aβ plaques.  What Are The Disadvantages Of Composites? for more information.