Spontaneous Exfoliation and Osteonecrosis Following Herpes Zoster Infection in an HIV-Seropositive Subject: A Case Report

    

    

    Figure 3:  Empty socket.
    
    

Discussion

Zoster is a common, predominantly dermal, and neurologic disorder caused by the varicella-zoster virus (VZV), a virus morphologically and antigenically identical to the virus causing

varicella (chickenpox). Difference in clinical manifestations between varicella and zoster apparently depends on the immune status of individual patients; those with no prior immunologic exposure to varicella virus, most commonly children, develop the clinical syndrome of varicella, while those with circulating varicella antibodies develop a localized zoster. Zoster probably results most often from a failure of the immune system to contain latent varicellazoster virus replication. Whether other factors such as radiation, physical trauma, certain medications, other infections, or stress also can trigger zoster has not been determined with certainty. Nor is it entirely clear why circulating varicella antibodies and cellmediated immune mechanisms do not prevent recurrent overt disease, as is common with most other viral illnesses [4]. Zoster most commonly manifests in 1 or more posterior spinal ganglia or cranial sensory ganglia, presumably because viral particles have been preserved within these ganglia in a dormant state since the original episode of varicella. This results in pain and characteristic cutaneous findings along the corresponding sensory dermatomes of the involved ganglia. Less often, involvement of anterior and posterior horn cells, leptomeninges, and peripheral nerves is observed, with consequent muscle weakness or palsy, pleocytosis of spinal fluid, and/or sensory loss. Rarely, myelitis, meningitis, encephalitis, or visceral involvement may occur [5]. Osteonecrosis following herpes zoster infection is a rare but severe complication, and clinicians awareness is important for early detection and management of this condition. The most significant and debilitating complication of herpes zoster is herpetic neuralgia that accompanies and may persist in 10-15% of all zoster patients, particularly those over 60 years of age. Herpes zoster (HZ), a sporadic infection with an estimated lifetime risk of 10-20%, occurs in all age groups, especially among individuals who have had varicella any time in the past, but its prevalence almost doubles in each decade past the age of 50 years [6]. Individuals with immunosuppression are also more prone to it. The most significant and debilitating complication of HZ is herpetic neuralgia that accompanies and may persist in 10-15% of all zoster patients, particularly those over 60 years of age. Cranial and peripheral nerve palsies, encephalitis, pneumonitis, acute retinal necrosis, encephalitis, myelitis, and secondary bacterial infection are other well-known complications of HZ. The described cases had an uncommon complication of spontaneous tooth exfoliation after trigeminal HZ, of which only about 39 cases have been reported before 2012 in the English literature [3]. The precise pathomechanism(s) of these oral complications eventually leading to tooth loss and necrosis of the alveolar bone, periodontal tissue membrane, nerve supply, and adjacent gingival tissue remain largely uncertain. The pre-existing local periodontal disease does not appear to influence the tooth loss [7]. Although the majority of the described cases are aged over 50 years, had severe HZ, were suffering from lymphoproliferative or other malignancies, HIV infection, receiving corticosteroids or chemo-/radiotherapy, the conditions well-known for increased incidence and severity of HZ, few of the reported cases have been young, immunocompetent, and otherwise healthy individuals suggesting that factors like old age, pre-existing systemic illnesses too seem not to precipitate this rare complication. It has been also postulated that it could result from intense vasoconstriction, endarteritis, or vasculitis with ischemia of the blood supply that may be caused by the virus migrating along the trigeminal neurovascular bundle. It is possible that the varicella zoster virus invades the sympathetic nerves that accompanying the blood vessels to the alveolar bone causing vasoconstriction and hampered blood supply or that systemic viral infection perhaps injures odontoblasts and cause degenerative tissue changes/pulp necrosis [6]. Another plausible explanation is that by direct extension of neural inflammation and edema, the adjacent alveolar artery may get compressed in the narrow bony channels and resultant poor tissue perfusion. The postulation of local vasculitis caused by varicella zoster virus leading to infarction and ischemia of the periodontal tissue and alveolar bone has limited evidence despite well-documented vascular damage it causes in the central nervous system [8,9]. It has been reported in a south African study that extensive osteonecrosis and exfoliation of teeth in the area innervated by the nerve affected by HZ was more common in HIV sero positives, and the patient reported here was also HIV positive [10]. Acyclovir has been proved to reduce the duration and severity and the course of the herpes zoster infection in the acute phase significantly, if treatment is initiated within 48 hours of the onset of the symptoms. Acyclovir is considered to be beneficial in treating zoster patients due to its increased rate of phosphorylation in herpes infected cells. The present case is treated on the same backgrounds [11].

Conclusion

The Varicella Zoster Virus (VZV) produces two clinical results: varicella or chickenpox and Herpes Zoster Infection (HZI). Herpes Zoster (HZ) presents as a cutaneous vesicular eruption in the area innervated by the affected sensory nerve, usually associated with severe pain. Oral manifestations of HZ appear when the mandibular or maxillary divisions of the trigeminal nerve are affected. Herpes zoster infection leads to various complications if left untreated. Severe osteonecrosis and exfoliation of teeth in the region innervated by the nerve affected by HZ has been reported after HZ infection. Oral physicians should have a thorough knowledge about this condition, the treatment and prevention of the complications.

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