| Abstract|| |
Herpes zoster is an uncommon acute viral infection caused by reactivation of varicella zoster virus. During the prodromal stage, the only presenting symptom may be odontalgia, which may prove to be a diagnostic challenge for the dentist. Practicing dentist may carry out emergency treatment that might result in irreversible damage or may delay the appropriate treatment. With an ever-increasing number of elderly and immunocompromised patients reporting to the dentist, the dental profession can expect to encounter an increased number of herpes zoster patients. Dentist must be familiar with the presenting signs and symptoms of patients experiencing the prodromal manifestations of herpes zoster of the trigeminal nerve. This article focuses on the difficulties in management of such cases, and one such case is reported here.
Keywords: Herpes zoster, odontalgia, reactivation, varicella zoster
|How to cite this article:|
Guttiganur N, Devanoorkar A, Aspalli S, Shetty S. Herpes zoster of trigeminal nerve after dental extraction. Indian J Dent Res 2013;24:396
Herpes zoster (HZ) is an acute viral infection caused by reactivation of varicella zoster virus (VZV). Following the primary varicella infection (chickenpox), typically in childhood, VZV establishes latency in dorsal root or cranial nerve ganglia.  Reactivation of VZV, although uncommon, results in its spread from the ganglion to the corresponding dermatome(s), producing neurocutaneous signs and symptoms - HZ or shingles.  HZ affecting the oral and maxillofacial region may pose a significant diagnostic challenge and should be considered in the differential diagnosis of those presenting with atypical odontalgia.  Other diagnoses in the early stages of symptoms may include irreversible pulpitis, acute periapical periodontitis, or even acute sinusitis. Prompt management is required, especially in immunocompromised individuals, to prevent complications, which may cause significant morbidity.  The practicing dentist must be familiar with the presenting signs and symptoms of patients experiencing the prodromal manifestations of HZ of the trigeminal nerve. The difficulties in management of such cases are discussed and one such special case is reported here.
|How to cite this URL:|
Guttiganur N, Devanoorkar A, Aspalli S, Shetty S. Herpes zoster of trigeminal nerve after dental extraction. Indian J Dent Res [serial online] 2013 [cited 2017 Nov 22];24:396. Available from: http://www.ijdr.in/text.asp?2013/24/3/396/118011
| Case Report|| |
A 65-year-old male patient reported to his dentist, complaining of recent onset of pain and discomfort relating to an upper central incisor tooth. His medical history was not significant; personal history revealed that he was a vegetarian, and by occupation he was a jewellery merchant. On intraoral examination, grade III mobility was noticed in relation to upper central incisor and rest of the teeth were also showing generalized mobility. Because of compromised periodontal health, patient had difficulty in chewing. Based on the clinical examination, diagnosis of generalized chronic periodontitis was made. Subsequently, the tooth was extracted under local anesthesia. The patient reported back to his dentist 3 days following the extraction with a complaint of painful swelling of the left side of his face, with tingling sensation and malaise. Clinical examination revealed a non-tender, diffuse edematous swelling with widespread erythema and crusting distributed over the left ophthalmic, maxillary, and mandibular divisions of the trigeminal nerve, exhibiting unilateral involvement without affecting the right side of the face [Figure 1]. No cranial nerve neuropathies were noted, with all other nerves being grossly intact. The left conjunctiva was inflamed, but acuity and pupillary reflexes were normal. Intraorally, vesicular eruptions, erythema and areas of ulcerations were noted unilaterally over the distribution of the maxillary and mandibular nerves, including the hard palate and buccal mucosa [Figure 2]. On questioning, it was found that patient had positive history of varicella zoster infection in his childhood. A provisional diagnosis of HZ of the trigeminal nerve was made and he was referred to dermatologist for further management. Dermatologist further confirmed the diagnosis of HZ of the trigeminal nerve and started acyclovir (ACV) course of treatment and followed up for the period of 1 month. Later, the patient presented after 1½ months with complete recovery of lesion [Figure 3].
|Figure 1: Unilateral involvement. Photograph showing facial swelling with erythema and crusting over the distribution of the left ophthalmic, maxillary, and mandibular branches of the trigeminal nerve|
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|Figure 2: Intraoral lesion. Photograph showing unilateral vesicles, erythema, and crusting affecting the hard palate and buccal mucosa|
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| Discussion|| |
The majority of HZ infections involve the thoracic and lumbar dermatomes; however, approximately 13% of patients present with infections involving any of the three branches of the trigeminal nerve.  The ophthalmic branch is most commonly affected; however, in our case, all the three branches of trigeminal nerve were involved.
Reactivation of VZV may occur spontaneously or when host defenses are compromised. Increasing age,  physical trauma  (including dental manipulation),  psychological stress, , malignancy,  radiation therapy,  and immunocompromised states including transplant recipients, immunomodulatory therapy, and HIV infection  are predisposing factors for VZV reactivation. The case reported here, as well as others with increased age, physical trauma  (including dental manipulation),  and psychological stress  exhibit an impaired host immune response which may contribute to the development of HZ.  Patients with HZ may progress through three stages: Prodromal stage, active stage (also called acute stage), and chronic stage. 
The prodromal stage presents as sensations (described as burning, tingling, itching, boring, prickly) occurring in cutaneous distribution of the dermatome and is believed to represent viral degeneration of nerve fibrils.  During this period, if branches of the trigeminal nerve are affected, odontalgia and pulpal necrosis may be seen. For the latter, it is proposed that the reactivated virus may travel the length of the nerve and infect the pulp vasculature leading to infarction and necrosis.  Furthermore, these symptoms may present up to 1 month before the acute mucocutaneous lesion, and pose significant diagnostic difficulties.
The active stage is characterized by the emergence of the rash which is nearly always accompanied by systemic upset. The characteristic skin rash progresses from erythematous papules and edema to vesicles and finally to pustules within 1-7 days which dry and crust and are exfoliated over 2-3 weeks, leaving erythematous macular lesions that may scar. Diagnostic difficulties may be encountered when the vesicular rash does not occur (zoster sine herpete).  Surprisingly, pain is reported to subside when the rash is most active; however, it returns during the crusting and scale phase until the rash clears.  It is during the active or "eruptive" phase that HZ is most contagious and could pose a significant cross-infection risk. The chronic stage is only seen in approximately 10% of all patients with HZ, and is termed post-herpetic neuralgia. It is described as a brief recurrent shooting or shocking allodynia, with a constant, usually deep pain, lasting beyond the period of healing of the active skin lesions. It may persist for years and is a significant cause of morbidity. Although post-herpetic neuralgia is the most common complication of HZ, other complications include neurological disorders, and ophthalmologic, cutaneous, and visceral complications;  immunocompromised individuals with HZ exhibit a significantly higher rate of complications. Periapical lesions, root resorption, tooth exfoliation, and alveolar osteonecrosis have also been reported in association with HZ infection.
Although HZ is a self-limiting condition and resolution is usually complete, treatment is indicated in some cases to reduce the acute symptoms of pain and malaise, to limit the spread and duration of the skin lesions, and to prevent complications.  The pharmacological approach is based on symptomatic relief and antiviral therapy. For many years, ACV has been the antiviral drug of choice for the treatment of VZV infections. Recently, other antiviral agents such as valaciclovir and famciclovir have been developed to overcome the low oral bioavailability of ACV and its limited and less predictable effect in preventing the development of post-herpetic neuralgia, as well as to provide a more favorable dosage regime.  Antiviral therapy should be initiated as early as possible, especially when patient factors that may complicate the manifestations of the condition are expected.
In the present case, dental treatment related stress and increased age would be the contributing factors for the reactivation of the varicella zoster; however, as the patient reported at an earliest stage to the dentist, the case was suspected for HZ and was referred to the dermatologist, where it was managed with antiviral drugs. The dentist plays an important role in identification of such cases at an early stage that would help in the early diagnosis and prompt treatment, thus decreasing the duration and complication of such viral infection.
| Conclusion|| |
A case of HZ affecting the trigeminal nerve is reported here. This case highlights the importance of a thorough dental history and examination in patients with odontalgia. In those presenting with atypical ondontalgia, HZ should be considered in the differential diagnosis. With an ever-increasing number of elderly and immunocompromised patients attending the dentist, the dental profession can expect to encounter an increasing number of HZ patients. The practicing dentist must be familiar with the presenting signs and symptoms of patients experiencing the prodromal manifestations of HZ of the trigeminal nerve. Furthermore, appropriate decision making and referral to the concerned specialist seems to be utmost important as seen in this case.
| References|| |
|1.||Owotude FJ, Ugboko VL, Kolude B. Herpes zoster infection of the maxilla: Case report. J Oral Maxillofac Surg 1999;57:1249-51. |
|2.||Schmader KE, Dworkin RH. Natural history and treatment of herpes zoster. J Pain 2008;9(1 Suppl 1):S3-9. |
|3.||Tidwell E, Hutson B, Burkhart N, Gutmann JL, Ellis CD. Herpes zoster of the trigeminal nerve third branch: A case report and review of the literature. Int Endod J 1999;32:61-6. |
|4.||Mustafa MB, Arduino PG, Porter SR. Varicella zoster virus: Review of its management. J Oral Pathol Med 2009;38:673-88. |
|5.||Millar EP, Troulis MJ. Herpes zoster of the trigeminal nerve: The dentists' role in diagnosis and treatment. J Can Dent Assoc 1994;60:450-3. |
|6.||West RJ. Dentistry, herpes zoster, and varicella. Br Med J 1970;3:222. |
|7.||Buchbinder SP, Katz MH, Hessol NA, Liu JY, O'Malley PM, Underwood R, et al. Herpes zoster and human immunodeficiency virus infection. J Infect Dis 1992;166:1153-6. |
|8.||Thomas SL, Hall AJ. What does epidemiology tell us about risk factors for herpes zoster? Lancet Infect Dis 2004;4:26-33. |
|9.||Wung PK, Holbrook JT, Hoffman GS, Tibbs AK, Specks U, Min YI, et al. Herpes zoster in immunocompromised patients: Incidence, timing, and risk factors. Am J Med 2005;118:1416. |
|10.||Strommen GL, Pucino F, Tight RR, Beck CL. Human infection with herpes zoster: Etiology, pathophysiology, diagnosis, clinical course and treatment. Pharmacotherapy 1988;8:52-68. |
Department of Periodontics and Oral Implantology, A.M.E.'s Dental College and Hospital, Raichur, Karnataka
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3]