Mandibular osteonecrosis and Ramsay Hunt syndrome following a case of herpes zoster.

Varicella zoster virus (VZV) is the agent that causes chicken pox, a common childhood infection that characteristically presents as vesicular rashes affecting the trunk and head. After the primary infection has resolved, VZV lies dormant in the spinal dorsal root ganglia or extramedullary cranial nerve ganglia until reactivation results in herpes zoster (shingles). The sensory nerves of the trunk, as in classic shingles, and the fifth cranial nerve, as in trigeminal zoster, are the most frequently affected. Shingles is an acute viral infection characterized by the appearance of painful unilateral vesicular rash usually restricted to a dermatomal distribution of a sensory nerve. The rash of shingles is usually preceded by pain and paresthesia. A rare, severe complication of the reactivation of VZV in the geniculate ganglion of the facial nerve is Ramsay Hunt syndrome (RHS). RHS is characterized by otalgia, vesicles in the auditory canal, and ipsilateral facial paralysis. An even rarer complication of VZV infection includes post-zoster osteonecrosis. This report documents a case of severe mandibular osteonecrosis and RHS after an outbreak of herpes zoster and treatment strategies.

Maxillary osteonecrosis and spontaneous teeth exfoliation following herpes zoster.

BACKGROUND: Reports of osteonecrosis and spontaneous tooth loss following herpes zoster infection of the fifth cranial are extremely rare. Only 39 previously recorded cases of post-zoster osteonecrosis have been found in the literature. The unusual feature of the case of interest to the dental surgeon is a rare complication of tooth exfoliation and maxillary osteonecrosis. CASE REPORT: This article reports a case of 52-year-old man with herpes zoster infection of the trigeminal nerve and related alveolar bone necrosis and teeth loss. The etiology and management of herpes zoster infection associated with destructive sequelae are discussed. DISCUSSION: Very few cases of osteonecrosis and spontaneous teeth exfoliation secondary to herpes zoster are found in the literature. The exact mechanism by which herpes zoster induces these destructive changes in the alveolar bone and teeth cannot be proposed. As Varicella zoster virus is an aneurotropic virus, the possible provoking factors may be the infection of the nerves innervating the periosteum or the chronic inflammatory changes in the form of adverse periodontal disease and delayed healing of the extraction sockets associated with compromised host resistance.

Unusual oral complications of herpes zoster infection: report of a case and review of literature.

A case of herpes zoster infection with unusual oral complications involving the mandibular division of the trigeminal nerve is presented. The post-herpetic complications of osteonecrosis, spontaneous exfoliation of teeth, and subsequent pathologic fracture of mandible in the absence of concurrent predisposing factors in a 65-year-old man are demonstrated. Forty-one cases with osteonecrosis and spontaneous exfoliation of teeth previously presented in the literature are reviewed. This is the first report of pathologic fracture after herpes zoster infection.

Spontaneous tooth exfoliation, maxillary osteomyelitis and facial scarring following trigeminal herpes zoster infection.

A case of trigeminal herpes zoster (HZ) infection affecting the left maxillary and ophthalmic divisions of the fifth cranial nerve in an immuno-competent patient is presented. Extremely rare complications such as osteonecrosis, spontaneous tooth exfoliation, secondary osteomyelitis and facial scarring were observed. Sequestrectomy, aciclovir and erythromycin stearate were effectively used in managing the case.

Alveolar bone necrosis and tooth exfoliation following herpes zoster infection: a review of the literature and case report.

BACKGROUND: 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. METHODS: This is a case report of a 63-year-old woman with HZ infection with trigeminal nerve involvement that led to a rapid loss of alveolar bone and exfoliation of two teeth. RESULTS: The initial intraoral examination showed redness of the alveolar mucosa and gingiva of the lower right quadrant with multiple well-delimited and painful erosive lesions affecting the attached gingiva around the teeth. Two weeks later, teeth number 27 (lower right canine) and 28 (lower right first premolar) had class III mobility, flow of purulent exudate from the gingival sulcus, and deep pockets (>11 mm). The radiological examination showed advanced alveolar bone loss around both teeth. The prognosis for teeth number 27 and 28 was considered hopeless, and they were extracted. Due to extensive necrosis there was no interdental alveolar bone. The case is presented with a review of clinical data from patients with trigeminal HZ infection associated with osteonecrosis or exfoliation of teeth previously reported in the literature. The mechanisms by which the HZ infection leads to the alveolar bone necrosis are discussed. CONCLUSIONS: Extensive osteonecrosis and exfoliation of teeth in the area innervated by the nerve affected by HZ has been reported after HZ infection. Clinicians should be aware of this possible outcome after a trigeminal HZ infection.

Tooth exfoliation, osteonecrosis and neuralgia following herpes zoster of trigeminal nerve.

A case of herpes zoster of the trigeminal nerve with complications of osteonecrosis and neuralgia in the absence of local or systemic predisposing factors is presented. The literature is reviewed and the role of varicella zoster virus in the pathology of tooth exfoliation and osteonecrosis is discussed.