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 Table of Contents  
Year : 2015  |  Volume : 5  |  Issue : 2  |  Page : 77-80

Herpes labialis in patient with periodontitis: A concomitant or exacerbating factor

1 Department of Periodontics, University of Benin, Benin City, Edo State, Nigeria
2 Department of Periodontics, University of Benin Teaching Hospital, Benin City, Edo State, Nigeria

Date of Web Publication28-Jan-2016

Correspondence Address:
Clement C Azodo
Room 21, Second Floor, Department of Periodontics, Prof. Ejide Dental Complex, University of Benin Teaching Hospital, P.M.B 1111 Ugbowo, Benin City, Edo State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2229-6360.175029

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The significance of herpes viruses in the causation and pathogenesis of periodontal diseases is not completely understood. However, the viral-bacterial association appears to be implicated in the development of periodontal diseases. The article was a report of herpes labialis in a patient with periodontitis as a concomitant or exacerbating factor. This article reported a case of herpes labialis in an otherwise healthy 59-year-old female with Miller Grade I mobility of 47 associated 5 mm periodontal pocket and severe pain. Subgingival scaling, root planning, and grinding of the nonfunctional cusp of affected tooth was done under local anesthesia. The periodontal dressing was applied, analgesics and antibiotic medication prescribed, warm saline mouth bath and oral hygiene instruction given before discharge. On recall, complete resolution of pain, tooth mobility, and herpes labialis were noted. In conclusion, herpes labialis may be considered as a potential periodontitis exacerbating or concomitant factor if it occurs before or at same time, respectively. Assessment of symptoms of herpes labialis and evaluation of herpes simplex-1 antibodies in periodontitis patients of the negroid race presenting with pain is recommended.

Keywords: Herpes labialis; scaling and root planning; triggering factors

How to cite this article:
Azodo CC, Uche IE. Herpes labialis in patient with periodontitis: A concomitant or exacerbating factor. Indian J Multidiscip Dent 2015;5:77-80

How to cite this URL:
Azodo CC, Uche IE. Herpes labialis in patient with periodontitis: A concomitant or exacerbating factor. Indian J Multidiscip Dent [serial online] 2015 [cited 2022 Aug 13];5:77-80. Available from: https://www.ijmdent.com/text.asp?2015/5/2/77/175029

  Introduction Top

A periodontal disease is a disease affecting one or more components of the periodontium which include gingiva, cementum, periodontal ligament, and alveolar bone. The major etiological factor for this disease is dental plague which is composed majorly of microorganism. The microbial constituents of plaque are mainly bacteria which are indisputable precipitants of periodontal disease directly through toxin, enzymes, and toxic metabolic product release and indirectly through antigen-antibody complexes and complement activation after overcoming the host defense. The other nonbacterial microbial constituents of plaque are virus, fungi, protozoa, and mycoplasma. The noted periodic exacerbation and remission characteristics of periodontal disease suggest that the presence of other organisms may contribute to the disease.

In recent times, different viruses have been implicated in the pathogenesis of periodontal disease among which is the herpes viruses. Herpes virus has been reported to be involved in the onset and progression of some periodontal diseases while human immunodeficiency virus (HIV) is related to linear gingival erythema and necrotizing ulcerative periodontitis.[1]

Herpes virus which are usually composed of a double-stranded DNA genome surrounded by nucleocapsid and lipid envelope, represent some of the most successful viruses in humans, infecting over 90% of humans and persisting for the lifetime of the affected individuals.[2] They are considered as the most important DNA viruses in dental practice because of their orofacial manifestations. Herpes viral activation markers have been detected from the crevicular fluid of periodontal lesions while the viral DNA has been isolated from gingival tissue, cervicular fluid, and subgingival plaque of the periodontally diseased sites. These explain why they are commonly found in periodontal pockets where they are considered to cause disease either as a direct result of the virus activity or as a result of viral-induced host defense impairment. Herpes virus-mediated periodontopathogenicity operating either alone or in combination has been stated to include suppression of periodontal immune defenses, the overgrowth of periodontal bacterial pathogens, the release of proinflammatory cytokines and chemokines and the initiation of cytotoxic or immunopathological events.[3],[4]

Herpes simplex virus-1 (HSV-1), HSV-2, varicella-zoster virus, Epstein-Barr virus (EBV), human cytomegalovirus (HCMV), human herpes virus-6, human herpes virus-7, and human herpes virus-8are the identified herpes virus so far. HSV-1 is very common herpes virus that affects the upper aerodigestive tract with the most common primary clinical manifestations as herpetic gingivostomatitis and pharyngitis and herpes labialis as the most common recurrent clinical manifestations. HSV-1 has been documented to induce mental nerve neuropathy which occurred as a result of inferior alveolar nerve infection through an extraction wound.[5] HSV infection has also been proposed as the etiological factors of different tumors, including breast cancer, thyroid cancer, and lymphomas.[6] HSV-1 with HCMV and EBV have emerged as putative pathogens in aggressive periodontitis. However, it is the HCMV and EBV have been reported to play important roles in the aetiopathogenesis of severe types of periodontitis because of their presence in high frequency in adults with progressive periodontitis, different forms of aggressive periodontitis, HIV-associated periodontitis, acute necrotizing ulcerative gingivitis, periodontal abscesses, and some rare types of advanced periodontitis associated with medical disorders.[3],[7] The review of the literature did not reveal any report of herpes labialis infection in patient with periodontitis. A case of herpes labialis in a patient with periodontitis as a concomitant or exacerbating factor is hereby reported.

  Case Report Top

A 59-year-old female Bini trader, who presented with a week history of the hole on a tooth and severe, throbbing and radiating pain in Periodontology Clinic of University of Benin Teaching Hospital, Benin City, Edo State, Nigeria. The pain was spontaneous in onset, associated with a headache, sleep disturbance, and temporarily relieved by ibuprofen. There was a history of shocking sensation from cold and hot drinks but resolved with the use of desensitizing toothpaste. She cleans her teeth once-daily with medium texture toothbrush. She is married in a polygamous setting with five children. She neither consumes tobacco nor drinks alcohol. Examination of the same side of the face with the symptomatic tooth revealed ulceration on the lower lip which was preceded by 5 days earlier by vesicles. Patient ascribed the lesion to fever. Diagnosis of herpes labialis was made based on the lesion on lower lip [Figure 1]. Intraorally, plaque score was 1, calculus score was 1, and oral hygiene score was 2 which is fair oral hygiene using the simplified oral hygiene index. Miller Grade 1 tooth mobility was detected on the distal aspect of 47 which bleeds on probing with associated 5 mm periodontal pocket and was also tender on percussion. Periapical radiography showed a horizontal bone loss. Diagnosis of localized chronic periodontitis was made. Scaling, root planning and occlusal grinding of the nonfunctional cusp of the involved tooth was done under local anesthesia using lidocaine. The periodontal dressing was placed over the operated site [Figure 2]. Oral analgesics in the form of ibuprofen (400 mg) was prescribed for 3 days while antibiotics in the form of amoxicillin (500 mg) and metronidazole (400 mg) were prescribed eight hourly daily for 5 days. On recall, there was the resolution of symptoms (periodontal and lip) and patient placed on twice yearly periodontal maintenance treatment [Figure 3] and [Figure 4].
Figure 1: Herpes labialis

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Figure 2: Periodontal dressing in situ

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Figure 3: Resoled herpes labialisv

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Figure 4: Improved periodontal condition clinically

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  Discussion Top

The heterogeneity of periodontal disease suggests that bacteria are unlikely to be the sole cause or modulator and the noted periodic exacerbation and remission characteristics of periodontal disease also suggest that the presence of other organisms may contribute to the disease. Although, the roles of virus in periodontal disease have not been completely understood, Grassi et al.[1] Reported that virus play a fundamental role in the development of periodontal disease as a result of their intrinsic capacity to alter their host immune system.

The complaint of the hole on the tooth by the patient in the absence of carious cavity is due to food packing in the periodontal pocket. The tooth mobility associated with 5 mm pocket and severe pain enough to cause sleep disturbance in this study signified acute exacerbation of the chronic periodontitis. A history of vesicular eruption few days after onset of the periodontal pain may invariably qualify the herpes labialis as the exacerbant factor of the periodontitis in this patient. The shedding of HSV-1 in herpes labialis with subsequent viral-periodontopathogenic bacterial interaction is suggested as being responsible. As it has been proposed by the herpes viral-bacterial hypothesis of periodontitis, that an active herpes virus infection initiates periodontal tissue breakdown and host immune responses against the herpes virus infection are an important component of the aetiopathogenesis of the disease. It can, therefore, be assumed that the localized periodontitis in this patients may be due to the elevated levels of periodontopathic bacteria reported by Saygun et al.,[7] Slots et al.[8] and Slots et al.[9] in herpes virus-associated periodontal sites which include Porphyromonas gingivalis, Tannerella forsythia, Dialister pneumosintes/Dialister invisus, Prevotella intermedia, Prevotella nigrescens, Treponema denticola, Campylobacter rectus, and Actinobacillus actinomycetemcomitans as impaired host defense resulting from immunosuppression, infection, physical trauma, hormonal changes, psychosocial, and physical stress which are herpes virus-activating factors, are also recognized risk indicators for periodontal disease.[10],[11] Based on the aforementioned, it means that herpes labialis and exacerbation of periodontitis can occur as concomitant events.

In herpes labialis, treatment is limited to emergency care and elective procedures are delayed until lesions are healed.[12] The spontaneity of patient's pain associated with a headache, sleep disturbance and temporarily relieved by ibuprofen is an indication for emergency care. Local microbial load reduction was done by root planning in conjunction with optimal doses of metronidazole and amoxicillin. The mechanical care reduced inflammation and prescribed analgesics which are anti-inflammatory in nature helps to arrest the pain complaints of the patient. This approach to care is also employed in other infective oral lesion like acute necrotizing ulcerative gingivitis.[13] Occlusal contact reduction achieved by occlusal grinding helped to reduce undue forces and facilitate healing. Prevention of microbial contamination of treated site was done by periodontal dressing application which also acted as a temporary splint for the mobile teeth. Periodontal dressing after nonsurgical periodontal treatment is beneficial in improving overall short-term clinical outcomes, and the probable mechanism is due to clot stabilization and prevention of bacterial colonization during wound healing.[14],[15] Further prevention of microbial contamination and increase in blood flow to the treated site to facilitate healing was the target of prescribed warm saline mouth and oral hygiene instruction. The rendered conventional (mechanical) and antimicrobial periodontal treatment reduced the periodontal load of herpes viruses thereby accounting for the positive treatment outcome on recall.[16],[17]

  Conclusion Top

Herpes labialis may be considered as a potential periodontitis exacerbating or concomitant factor if it occurs before or at same time, respectively. Assessment of symptoms of herpes labialis and evaluation of herpes simplex-1 antibodies in periodontitis patients presenting with pain is recommended.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Grassi FR, Pappalardo S, Frateiacci A, Scortichini A, Petruzzi M. Role of human viruses in the pathogenesis of periodontal disease. Minerva Stomatol 2003;52:211-7.  Back to cited text no. 1
Cohen JI. Epstein-Barr virus infection. N Engl J Med 2000;343:481-92.  Back to cited text no. 2
Slots J. Interactions between herpesviruses and bacteria in human periodontal disease. In: Brogden KA, Guthmiller JM, editors. Polymicrobial Diseases. Ch. 16. Washington, DC: ASM Press; 2002. p. 317-31.  Back to cited text no. 3
Feller L, Lemmer J, Meyerov R. The association between human herpesviruses and periodontal disease: Part 1. Herpesviruses immune evasion. A review. SADJ 2007;62:074, 076, 078-9.  Back to cited text no. 4
Yura Y, Kusaka J, Yamakawa R, Bando T, Yoshida H, Sato M. Mental nerve neuropathy as a result of primary herpes simplex virus infection in the oral cavity. A case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90:306-9.  Back to cited text no. 5
Di Crescenzo V, D'Antonio A, Tonacchera M, Carlomagno C, Vitale M. Human herpes virus associated with Hashimoto's thyroiditis. Infez Med 2013;21:224-8.  Back to cited text no. 6
Saygun I, Yapar M, Ozdemir A, Kubar A, Slots J. Human cytomegalovirus and Epstein-Barr virus type 1 in periodontal abscesses. Oral Microbiol Immunol 2004;19:83-7.  Back to cited text no. 7
Slots J, Sugar C, Kamma JJ. Cytomegalovirus periodontal presence is associated with subgingival Dialister pneumosintes and alveolar bone loss. Oral Microbiol Immunol 2002;17:369-74.  Back to cited text no. 8
Slots J, Kamma JJ, Sugar C. The herpesvirus-Porphyromonas gingivalis-periodontitis axis. J Periodontal Res 2003;38:318-23.  Back to cited text no. 9
Sculley TB, Apolloni A, Hurren L, Moss DJ, Cooper DA. Coinfection with A- and B-type Epstein-Barr virus in human immunodeficiency virus-positive subjects. J Infect Dis 1990;162:643-8.  Back to cited text no. 10
Nunn ME. Understanding the etiology of periodontitis: An overview of periodontal risk factors. Periodontol 2000 2003;32:11-23.  Back to cited text no. 11
Browning WD, McCarthy JP. A case series: Herpes simplex virus as an occupational hazard. J Esthet Restor Dent 2012;24:61-6.  Back to cited text no. 12
Atout RN, Todescan S. Managing patients with necrotizing ulcerative gingivitis. J Can Dent Assoc 2013;79:d46.  Back to cited text no. 13
Genovesi AM, Ricci M, Marchisio O, Covani U. Periodontal dressing may influence the clinical outcome of non-surgical periodontal treatment: A split-mouth study. Int J Dent Hyg 2012;10:284-9.  Back to cited text no. 14
Monje A, Kramp A, Criado E, Suárez-López Del Amo F, Garaicoa-Pazmiño C, Gargallo-Albiol J, et al. Effect of periodontal dressing on non-surgical periodontal treatment outcomes: A systematic review. Int J Dent Hyg 2015;doi: 10.1111/idh.12130.  Back to cited text no. 15
Saygun I, Sahin S, Ozdemir A, Kurtis B, Yapar M, Kubar A, et al. Detection of human viruses in patients with chronic periodontitis and the relationship between viruses and clinical parameters. J Periodontol 2002;73:1437-43.  Back to cited text no. 16
Slots J. Herpes viral-bacterial interactions in periodontal diseases. Periodontol 2000 2009;51:1-24.  Back to cited text no. 17


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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