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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 7  |  Issue : 3  |  Page : 184-186

Herpes zoster manifesting as isolated oral thin leukoplakia in an immunocompetent host


1 Department of Pathology, Sonoscan Healthcare, Malda, West Bengal, India
2 Department of Oral Pathology, North Bengal Dental College and Hospital, Darjeeling, West Bengal, India

Date of Web Publication22-Aug-2016

Correspondence Address:
Krishnendu Mondal
c/o Barendra Nath Mondal, Fularhat, P.O. and P.S. Sonarpur, South 24 Parganas - 700 150, West Bengal
India
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DOI: 10.4103/0976-433X.188810

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  Abstract 

Herpes zoster (HZ) has long been considered as a disease of immunocompromised elders. It is usually caused by the revitalized varicella; remaining dormant within the sensory ganglia of sacral dermatomes since an early childhood stint at chickenpox. Trigeminal nerve is rather uncommonly infested. Characteristic zoster lesions appear as unilateral mucocutaneous vesiculobullous rashes, preceded by intense radiating neuralgic pain for few days. This article emphasizes on an immunocompetent man, in his early sixties, presenting with two painful leukoplakic patches over buccal mucosa as the sole manifestation of HZ.

Keywords: Dermatome, exfoliative cytology, herpes zoster, oral leukoplakia, varicella


How to cite this article:
Mondal K, Mandal R, Sarkar BC. Herpes zoster manifesting as isolated oral thin leukoplakia in an immunocompetent host. SRM J Res Dent Sci 2016;7:184-6

How to cite this URL:
Mondal K, Mandal R, Sarkar BC. Herpes zoster manifesting as isolated oral thin leukoplakia in an immunocompetent host. SRM J Res Dent Sci [serial online] 2016 [cited 2019 Nov 22];7:184-6. Available from: http://www.srmjrds.in/text.asp?2016/7/3/184/188810


  Introduction Top


Primary varicella, i.e., “chickenpox” prevails worldwide. Mostly children from 4 to 10 years of age group get infected. In 2010, around 6,800 people died of chickenpox, declining from 11,200 in 1990.[1] Yearly 0.1–0.4% immunocompetent children succumb to chickenpox, compared to a massive 15% for immunocompromised children.[2]

The causative virus insinuates through respiratory mucosa to regional lymph nodes, and then via mononuclear cells, it disseminates to flourish the characteristic mucocutaneous manifestations of chickenpox. Following the primordial resolution, the organism remains dormant within sensory ganglia; only to reactivate in the form of herpes zoster (HZ), during older years and/or immunosuppressed state. Only 10–20% individuals experience such a viral rejuvenation.[3]

Amidst all branches of the trigeminal nerve, the ophthalmic division is most commonly involved by HZ. Rare involvement of the maxillary and mandibular branches gives rise to painful oral blisters, ulceration, and notoriously the “oral hairy leukoplakia” in HIV/AIDS patients. However, zoster dissemination as isolated oral thin leukoplakia is unusual.[3]

Herein, we narrate a case of HZ in a 63-year-old immunosufficient patient presenting with painful leukoplakia over buccal mucosa.


  Case Report Top


A 63-year-old aged man presented to the outpatients clinic of oral pathology with two agonizingly painful thin white patches over buccal mucosa adjacent to his right oral commissure, since previous 10 days [Figure 1]. Mucosal blistering, ulceration, any other cutaneous manifestations, or relevant constitutional symptoms were absent. He also complained that the patches were preceded by the radiating pain by about 24 h. Neither was he addicted to any tobacco products, alcohol; not having an ill-fitting denture or spicy dietary habits. Any related history indicative of ongoing immunosuppression was negative. His oral hygiene was pleasurable as well. Failing to explain its exact causality, the lesion was primarily stamped as “oral leukoplakia” and subjected to additional diagnostic work-ups.
Figure 1: Oral herpes zoster: Clinically, two leukoplakic patches (arrows) over buccal mucosa

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The patch was sampled for exfoliative cytological examination using a conventional wooden spatula. The smears were stained with Papanicolaou stain and examined under light microscope. Cytologically, these smears were paucicellular, comprised by a population of morphologically altered squamous epithelial cells, appearing in small groups as well as in singles. These cells exhibited uniform cytomegaly and karyomegaly without much alteration in overall nuclear-cytoplasmic ratio. Their nuclei appeared glassy homogeneous and faintly basophilic with thickened nuclear membrane [Figure 2]a. Occasionally, the nuclei contained solitary, large, brightly eosinophilic-to-dark purple, round-to-oval intranuclear inclusions; well separated from the nuclear membrane by a clear halo. Nucleoli were absent. Cytoplasm stained condensed cyanophilic. Few multinucleated giant cells were also present that contained multiple overlapping molded nuclei alongside the intranuclear inclusions [Figure 2]b. At times, the nuclei assumed a bizarre configuration, simulating certain neoplastic pathogenesis. However, the absence of significant nuclear pleomorphism, chromatin coarseness, or background diathesis strongly negated such possibility.
Figure 2: Oral herpes zoster: Cytologically, uniform nucleocytomegaly with normal nuclear-cytoplasmic ratio, thickened nuclear membrane, glassy homogeneous chromatin, inconspicuous nucleoli (a) and round-to-oval deep eosinophilic-to-dark purple intranuclear inclusions (black arrows) separated from nuclear membrane by a halo. (b) Multinucleated giant cells (b, inset) with nuclear molding and intranuclear inclusion (white arrow) also present (Pap, ×400)

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Considering the overall cytomorphology in the backdrop of classic clinical presentation, reinforced by the childhood history of chickenpox virtually clinched the diagnosis of HZ. The patient was promptly instituted upon oral acyclovir, analgesics, and Vitamin B complex; which gradually provided him with symptomatic relief and resolution of the oral lesions within a week.


  Discussion Top


HZ can develop at any age. However, its incidence increases with age and deteriorating immunity. Its prevalence reaches 50% beyond 50 years and >70% after the seventh decade.[4] Zoster revives in about 20% personnel, usually decades afterward. Immunodeficit hosts though get infected much earlier, often within a year or two of earlier contact with chickenpox.[5] The discussed patient was in his sixties and was not immunocompromised as well. Moreover, he manifested the zoster symptoms ages past his childhood ailments.

Varicella-zoster virus has the supreme quality to infect both skin and nerves plus can also commence latent infection within any sensory ganglia.[2] Dermatomes from T3-L2 are mostly affected with HZ. In only 13% cases, the trigeminal nerve is invaded with the ophthalmic division suffering its dominant share.[6] Zoster-associated late but virulent complications include various neurological and ocular catastrophes.[7] The presently discussed patient had only two small painful leukoplakic patches over buccal mucosa corresponding to mandibular dermatome of the trigeminal. No other related lesion or complication bothered him during this illness.

Ideally, HZ advances through three stages: (i) Prodromal, (ii) active or acute, and (iii) chronic. The prodromal stage is characterized by paresthesia, anesthesia, or severe neuralgic pain. Active stage is most lengthy, persists for weeks. It is characterized by erythematous rash, vesicles, etc., plus the constitutional symptoms. The chronic pain stage is popularly known as “postherpetic neuralgia,” when radiating pain sustains beyond the resolution of rashes.[6],[7] However, rare patients fail to progress through all three successive stages. Barrett et al.[8] experienced trigeminal neuralgia in the absence of any vesiculobullous eruption as the sole manifestation of HZ in their report. Likewise, in the present illustration, classical herpetic rash, or ulceration was absolutely absent.

Diagnosis of HZ is usually accomplished from clinical perspectives. Absence of vesicular rash sometimes complicates the diagnostic challenge. This dilemma can be effectively settled by various confirmatory tests.[7] These include cell culture or demonstration of varicella antigens, antibodies, nucleic acids by polymerase chain reaction, immunofluorescent techniques, etc.; or observation of characteristic varicella-induced cytopathic effects on cytology or histology.[9] In this respect, Barrett et al.[8] were compelled to employ culture methods for confirmation of HZ. On the contrary, Tidwell et al.[7] undoubtedly relied upon simultaneous history and clinical features in diagnosing HZ, despite the continuous absence of prototypical rashes. However, similar to the discussed case, Kar et al.[10] also successfully identified the signature cytopathic changes induced by HZ in diagnosing their case.

Differential clinical considerations of oral white patches as in the current case include oral candidiasis, lichen planus, frictional keratosis, chemical injury, smokers' keratosis, and primary herpes simplex infection.[11] However, implicit notification of personal history and presenting symptoms, physical appearance of the lesion, and the self-explanatory cytologic findings estranged the reported case from its clinical mimickers. Although cytologically herpes simplex and zoster lesions are indistinguishable from each other, the typical sensory dermatome involvement strongly favored the zoster shingles in the present case.[3]


  Conclusion Top


Painful oral thin leukoplakia is a rare manifestation of HZ. Various other pathologies often tangle up diagnostic concern, especially when the characteristic rashes are lacking. However, meticulous evaluation of history and clinicopathological features yields the diagnosis of HZ.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: A systematic analysis for the global burden of disease study 2010. Lancet 2012;380:2095-128.  Back to cited text no. 1
    
2.
Dwyer DE, Cunningham AL. 10: Herpes simplex and varicella-zoster virus infections. Med J Aust 2002;177:267-73.  Back to cited text no. 2
    
3.
Brooks GF, Carroll KC, Butel JS, Morse SA, editors. Herpes viruses. In: Jawetz, Melnick and Adelberg's Medical Microbiology. 25th ed. New York: Lange Medical Books/McGraw-Hill Companies; 2010. p. 452-8.  Back to cited text no. 3
    
4.
The French Society of Infectious Diseases. Consensus conference: Management of infections due to the varicella zoster virus. Méd Mal Infect 1998;28:1-8.  Back to cited text no. 4
    
5.
Ragozzino MW, Melton LJ 3rd, Kurland LT, Chu CP, Perry HO. Population-based study of herpes zoster and its sequelae. Medicine (Baltimore) 1982;61:310-6.  Back to cited text no. 5
    
6.
Millar EP, Troulis MJ. Herpes zoster of the trigeminal nerve: The dentist's role in diagnosis and management. J Can Dent Assoc 1994;60:450-3.  Back to cited text no. 6
    
7.
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.  Back to cited text no. 7
    
8.
Barrett AP, Katelaris CH, Morris JG, Schifter M. Zoster sine herpete of the trigeminal nerve. Oral Surg Oral Med Oral Pathol 1993;75:173-5.  Back to cited text no. 8
    
9.
Forbes BA, Sahm DF, Weissfeld AS. Laboratory methods in basic virology. In: Wilson L, editor. Bailey & Scott's Diagnostic Microbiology. 12th ed. Missouri: Mosby Elsevier; 2007. p. 749-59.  Back to cited text no. 9
    
10.
Kar HK, Gautam RK, Jain RK, Puri P, Doda V. Disseminated cutaneous herpes zoster: A clinical predictor of human immunodeficiency virus infection. Indian J Dermatol Venereol Leprol 1995;61:40-1.  Back to cited text no. 10
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11.
Warnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa. J Oral Pathol Med 2007;36:575-80.  Back to cited text no. 11
    


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