Alveolar bone necrosis and tooth exfoliation secondary to herpes zoster in the setting of HIV/AIDS

Abstract

Varicella–Zoster virus (VZV) is one of the eight herpesviruses that have been found to affect humans, and is the cause of both varicella (chicken pox) and herpes zoster (shingles). Unlike varicella, herpes zoster is a sporadic disease with a lifetime risk estimated to be 10–20%. Herpes zoster can occur in anyone who has had varicella, but is more common with increasing age, almost doubling in each decade past the age of 50 years. It is also more frequent in immunocompromised patients. Other complications of herpes zoster are widespread, and include postherpetic neuralgia, encephalitis, myelitis, cranial and peripheral nerve palsies, secondary bacterial infection, acute retinal necrosis and pneumonia [1]. A well-documented but rare complication of herpes zoster is spontaneous exfoliation of the teeth with alveolar bone necrosis [2]. Although some of these patients received chemotherapy for an underlying malignancy, relatively few cases of alveolar bone necrosis as a complication of herpes zoster have been described in HIV-positive patients [3,4]. Over a period of one year, six HIV-positive patients aged 36, 38, 47, 48, 52 and 73 years presented with skin and oral lesions after acute herpes zoster infection affecting the areas innervated by the mandibular division of the trigeminal verve. The patients presented with unilateral alveolar necrosis of the mandibular alveolar bone with sparing of the inferior border (Fig. 1). Three patients had sustained pathological fractures as a result of the loss of alveolar bone. Tooth exfoliation was present in the affected areas. The CD4 cell counts were available for four of the patients, which were all less than 200 cells/μl. No patient had a previous history of herpes zoster. Histological examination of the necrotic bone confirmed the presence of osteonecrosis without contributing towards the possible pathogenesis.Fig. 1: Unilateral alveolar bone necrosis ending abruptly in the midline. The tooth sockets from the exfoliated teeth are clearly visible.The EC-Clearinghouse consensus report is still the most widely used classification of oral lesions associated with adult HIV infection [5]. This scheme groups lesions into three categories according to the strength of association with HIV infection. This scheme is recognized to be more applicable to patients in Europe and the United States, with the need to document new and emerging oral diseases and conditions from developing countries emphasized [6]. Although herpes zoster is listed as a group 2 lesion (less commonly associated with HIV infection), spontaneous bone necrosis as a complication of herpes zoster is not listed in the classification. The alveolar bone of the maxilla and mandible has a rich vascular supply. It is derived from supraperiosteal arterioles, vessels from the periodontal ligament and vessels supplying the interdental bone crest. The precise mechanism of herpes zoster-related alveolar bone necrosis is still uncertain. The alveolar arteries may become compressed by the transudate associated with inflammation of the alveolar nerves in enclosed bony channels, with resulting ischaemia and necrosis of the alveolar bone and periodontium. A related postulate is that VZV may cause vasoconstriction of the blood vessels supplying the alveolar bone by invading the sympathetic nerves that accompany these vessels [2]. Evidence of local vasculitis in herpes zoster is limited, although extracranial granulomatous vasculitis has been reported as a postherpetic reaction whereas vascular damage by VZV in the central nervous system is well documented [7]. We have only encountered this manifestation of herpes zoster infection in the setting of HIV/AIDS, strengthening our opinion that alveolar bone necrosis as a complication of herpes zoster infection warrants inclusion as a group 2 lesion.