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Herpes Zoster and Relevant Comorbidity 

Introduction

Reaching a correct diagnosis in Endodontics can be as simple as placing a tetrafluoroethane saturated cotton on a suspect tooth and generating an unmistakeable response of either pulpal necrosis or symptomatic irreversible pulpitis. However, there are instances in which patients present with other non-odontogenic symptoms that mimic these common endodontic ailments that create difficulties for practitioners.

Varicella Zoster Virus (VZV) specifically is a DNA envelope virus only found in humans. Herpes Zoster is 1 of a total of 9 distinct viruses of the herpesviridae family. Typically 8 herpesviruses, 8 normally infect only humans, of the more than 100 known; varicella-zoster virus, Herpes simplex virus types 1 and 2, cytomegalovirus, Epstein-Barr virus, human herpesvirus 7 (variants A and B), human herpesvirus 6, and human herpesvirus 8 (KS). A simian virus, called B virus, is also capable of  infecting humans. All herpesviruses are effective at establishing latent infection within specific tissues, which are attributes for each virus. Herpesviruses have a unique four-layered structure: a core containing the large, double-stranded DNA genome is enclosed by a polyhedron capsid which is composed of capsomeres. A glycoprotein-bearing lipid bilayer envelope cases the capsid which is encircled by a tegument, which is simply an amorphous protein (Whitley 1996). With respect to varicella zoster virus (VZV), most patients that typically have this virus were infected at some earlier point in their life.  Normally after the virus accomplishes primary infection, it then continues dormant within the neural tissues, more specifically, ganglia tissue. Additional flare ups of herpes zoster typically surface after several years of latency, many times decades, when humans develop immunodeficiencies.

Epidemiology

  From and epidemiological standpoint, roughly over 1 million incidents of herpes zoster occur on an annual bases in the United States with a  lifetime risk that has been calculated to be as much as 10%–20%.  Immunosuppression, alcohol abuse, older age, radiation, treatment with any cytotoxic drugs, malignancies, and dental treatment are all potential risk factors for worsening of symptoms. Herpes zoster has been casually connected to stress, similarly too HSV1 and HSV2. A case-control study performed was able to document and show that if stressful life moments occurred, there would be an associated episode of herpes zoster within a 6 month period. Another cohort study, did however, show a nonsignificant association between stress life moments and subsequent episodes of herpes zoster (CDC 2008).

Most people usually experience only one incidence of herpes zoster in their  entire lifetime although recurrent episodes are not uncommon. A cohort study compared the incidence of herpes zoster recurrence between immunocompetent adults aged greater than or equal to 60 years who were or were not vaccinated following an episode of herpes zoster. It is hypothesized that the incidence of herpes zoster is associated with a reduction below an unknown, conceivably host-specific, threshold level of varicella zoster virus (VZV)–specific cell-mediated immunity. The data from this study supported that recurrences of herpes zoster are relatively uncommon in immunocompetent persons. The vaccinated group did show a lower incidence of recurrent episodes but the overall data when considered did not show a definitive benefit to have patients receive a vaccine (Tseng 2012). However, the current Advisory Committee Immunization Practices (ACIP) is recommending scheduled vaccination of all people 60 years or older with 1 dose of zoster vaccine. There is also no contraindication for people who report a previous history 
of zoster and those with any chronic medical conditions such as chronic renal failure, diabetes mellitus, rheumatoid arthritis, and chronic pulmonary disease; unless a contraindication can be determined for that particular patient (CDC 2008). 

Moreover, with regards to vaccination, the CDC and Advisory Committee Immunization Practices (ACIP) have made multiple recommendations with regards to patients who present with a compromised immune system. Herpes Zoster vaccine should be avoided in individuals presenting with malignant neoplasms affecting bone marrow and/or the lymphatic system such as leukemia and lymphoma. Individuals with AIDS or other clinical manifestations of HIV, including those with a CD4+ counts of less than 200. Any individuals undergoing immunosuppressive therapy, especially those prescribed high dose corticosteroids. Lastly, during pregnancy vaccination for herpes zoster should be avoided due to unknown potential effects on the fetus (CDC 2008).

Pathogenicity

With respect to varicella zoster virus (VZV), most patients that typically have this virus were infected at some earlier point in their life.  Normally after the virus accomplishes primary infection, it then continues dormant within the neural tissues, more specifically, ganglia tissue. Additional flare ups of herpes zoster typically surface after several years of latency, many times decades, when humans develop immunodeficiencies. It has the potential to affect any sensory ganglion and its associated nerve, commonly affecting more cranial nerve dermatomes than other thoracic and abdominal. The disease typically manifests by the appearance of a rash consisting of macules/papules in neighboring dermatomes, which usually maintain and ipsilateral disturbution. The rash progresses  into painful clusters of vesicles that proceed to form over approximately 4 days and eventually a dry crust over a couple of weeks to a month later. Incidence of the disease in immunocompromised individuals results in a rash that may affect 3 or more dermatomes.  Usually with maxillofacial active states, the trigeminal nerve (CN V) is the most common cranial nerve associated (approximately 20% of cases) followed by the glossopharyngeal (CN IX) and hypoglossal nerve (CN XII) . For cases involving the trigeminal (CN V), herpes zoster usually affects sections associated with the different branches and their respective dermatones; ophthalmic (V1), maxillary nerve (V2), and the mandibular nerve (V3).  Sometimes multiple dermatomes may be affected simultaneously regardless of 
immunocompetence. Most often reported involvement is the ophthalmic V1 dermatome, with the V2 and V3 dermatomes usually less commonly involved (Paquin et al. 2017). 

Diagnosis

The progression of herpes zoster infections is most easily described by three stages: a prodromal, active and a chronic stage; with some cases remaining completely asymptomatic. Burning, tingling, itching, boring, prickly or knife-like are typically descriptions of what patients encounter within the skin of the associated nerve distribution at the prodromal stage. More subjective clinical findings can be seen during the active stage of the disease. Usually the development of a rash with accompanied general malaise, headache and low-grade fever. Rash emergence will typically progress into eruption of erythematous papules leading to vesicles. Lastly, development of post herpetic neuralgia is possible in which a chronic pain lingers beyond healing of lesion that emerged during the active stage.

Relevant Comorbidity

Interestingly enough herpes zoster may present initially as odontogenic pain. This possible odontalgia presenting as pulpitis is challenging during the  prodromal stage of the disease for many physicians and dentist as it can be masked prior to the eruption of vesicles and rash (14–16) . Sometimes a differential diagnosis of orofacial pain associated with the trigeminal nerve may be further complicated by zoster sine herpete, which is basically the absence of clinically visible signs and symptoms, such as a vesicular rash during the active stage of the disease. The active stage associated with the emergence of rash accompanied by generalized malaise, headache, low grade fever and sometimes nausea. In this condition, dentist or physicians should typically suspect possible virological involvement and request serological testing for varicella zoster virus deoxyribonucleic acid or anti-varicella zoster virus antibodies in the serum or cerebrospinal fluid to establish a proper diagnosis as apposed to proceeding with unnecessary dental treatment such as root canal therapy (Paquin et al. 2017) 

Some patients may experience the pain associated with herpes zoster of the trigeminal nerve for months to even years after the physical signs and symptoms have has resolved. This resulting painful condition, post herpes zoster, is known as postherpetic neuralgia, and it happens to be the most common post-infectious ailment of herpes zoster. Myelitis, meningoencephalitis, and varicella zoster virus vasculopathy are possible concomitant complications of varicella zoster virus reactivation in herpes zoster. Therefore, cerebral infarction and stroke are possible delayed risks for patients with herpes zoster involving any trigeminal division. As far as endodontics is concern, pulpal or periapical pathosis associated with herpes zoster of the orofacial region have been reported during the course of the disease with debatable reasons of how the 2 sequelae are linked. More specially, case reports in the literature of multiple devitalization of four of five teeth in left maxillary quadrant in a 70-year-old woman with a history of herpes zoster infection affecting maxillary branch of the trigeminal nerve. In additions, reports non-vital teeth affecting entire left maxillary dentition except central incisor who suffered 8 years earlier herpes zoster involving maxillary division of the trigeminal nerve on the left side. External or internal root resorption, osteonecrosis of the jaw, and spontaneous exfoliation of teeth have been describe as other possible dental complications (Paquin et al. 2017).

Spontaneous exfoliation is a particular rare phenomenon that can occur as a result of an episode of herpes zoster. The time interval between the actual outbreak of herpes zoster infection and the spontaneous exfoliation of teeth in the area innervated by the affected nerve is currently still mystery that will require further investigation and hopeful publication in the literature. Alveolar bone necrosis, as well as, necrosis of the periodontal ligament may be accredit to the unexpected exfoliation of teeth. However, it is still unpredictable as to how exactly herpes zoster infection is directly related to the alveolar bone necrosis. Researchers have considered the possibility that local vasculitis perhaps could be it be caused by direct progression of the neural inflammatory process to adjacent blood vessels. Also, possible infarction of trigeminal vessels that travel with the trigeminal vessels that innervate the jaws or generalized infection of the trigeminal nerves supplying the periosteum and periodontium of the involved dermatome area.(Kaur 2017).
 
 

Prodromal Herpes Zoster and Odontalgia

The above images demonstrate a case reported in the endodontic literature by Paquin et al. This case report sheds additional light on the possible concomitant manifestations of herpes zoster. The patient presented with a “shooting pain”  radiating to his upper lip and right eye pain which began 5  before his appointment. Right Maxillary canine was diagnosed with pulp necrosis and symptomatic apical 

periodontitis was made. A few days post endodontic therapy, clinical signs and symptoms of  herpes zoster began to manifest. 

In the previously mentioned case, the tooth involved was diagnosed, as stated before, with pulp necrosis and symptomatic apical periodontitis. Dental pulp necrosis has been proposed as a mechanism for dental pulps undergoing Spontaneous necrosis during a herpetic outbreak within the trigeminal nerve has been proposed to be directly a result of dental pulp tissue undergoing focal dental pulp necrosis. The significance of a meticulous clinical examination as well as extensive pulp testing for guiding treatment decisions should be highly emphasized. Delaying treatment of odontalgia if there are no clinical findings such as percussion sensitivity, intra-oral or extra-oral swelling, purulent drainage, or radiographic periapical pathology is the most appropriate course to take for any patients affected by zoster who present with irreversible pulpitis pulpitis.  (Paquin et al 2017).

Management

Administration of antiviral therapy with acyclovir, famcyclovir, or valacyclovir in combination with prompt diagnoses of herpes zoster is truly the key.Starting of antiviral therapy early in the course of the disease may have beneficial in reduction of healing time and level of lesion manifestation. (Paquin et al. 2017). Research has show in controlled trials, that truly a decreased duration of skin symptoms and pain associated with herpes zoster could be demonstrated with a systemic use of acyclovir  and famcyclovir.A meta-analysis of four placebo-controlled trials of oral acyclovir showed  statically significant advantage over the control group regarding time to termination of pain (Werner et al 2017).

Over-the-counter analgesics are often do not provide adequate pain control, so prescription NSAIDS or narcotic analgesics should be considered. Prescriptions of oxycodone and gabapentin have also shown efficacy in pain reduction in association with acute herpes zoster.Tricyclic antidepressants (TCA), are also beneficial for the treatment of postherpetic neuralgia (Paquin et al). An ophthalmologic reassessment should be made by an ophthalmologist in a case of herpes zoster ophthalmicus. Possible acute retinal necrosis (ARN) can result from herpes zoster ophthalmicus. This is without question an ophthalmic emergency that has to be closely managed  by the proper credential physician to avoid severe consequences. Corticosteroids in the absence of antiviral medication should be prescribe with caution in order to avoid promotion of additional viral replication and possibly initiating or exacerbating acute retinal necrosis (Werner et al 2017).