Case Report

Herpes labialis in patient with periodontitis: A concomitant or

exacerbating factor
ABSTRACT
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.

Key words: Herpes labialis; scaling and root planning; triggering factors

Introduction exacerbation and remission characteristics of periodontal

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
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DOI:
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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
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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.

Clement C Azodo, Ifeyinwa E Uche1

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

Address for correspondence: Dr. 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, Nigeria. E‑mail: clementazodo@yahoo.com

© 2015 Indian Journal of Multidisciplinary Dentistry | Published by Wolters Kluwer - Medknow 77

 Azodo and Uche: Herpes as a concomitant or exacerbating periodontitis factor
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‑8 are 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
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
78 Indian Journal of Multidisciplinary Dentistry / Jul-Dec 2015 / Volume 5 / Issue 2
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 [Figures 3 and 4].
Discussion
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
Figure 1: Herpes labialis
 Azodo and Uche: Herpes as a concomitant or exacerbating periodontitis factor
Figure 2: Periodontal dressing in situ
Figure 3: Resoled herpes labialisv
Figure 4: Improved periodontal condition clinically
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.
Indian Journal of Multidisciplinary Dentistry / Jul-Dec 2015 / Volume 5 / Issue 2
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
79
 Azodo and Uche: Herpes as a concomitant or exacerbating periodontitis factor
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
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.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
1. Grassi FR, Pappalardo S, Frateiacci A, Scortichini A, Petruzzi M. Role
of human viruses in the pathogenesis of periodontal disease. Minerva
80 Indian Journal of Multidisciplinary Dentistry / Jul-Dec 2015 / Volume 5 / Issue 2
Stomatol 2003;52:211‑7.
2. Cohen JI. Epstein‑Barr virus infection. N Engl J Med 2000;343:481‑92.
3. 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.
4. 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.
5. 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.
6. 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.
7. 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.
8. 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.
9. Slots J, Kamma JJ, Sugar C. The herpesvirus‑Porphyromonas
gingivalis‑periodontitis axis. J Periodontal Res 2003;38:318‑23.
10. 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.
11. Nunn ME. Understanding the etiology of periodontitis: An overview of
periodontal risk factors. Periodontol 2000 2003;32:11‑23.
12. Browning WD, McCarthy JP. A case series: Herpes simplex virus as an
occupational hazard. J Esthet Restor Dent 2012;24:61‑6.
13. Atout RN, Todescan S. Managing patients with necrotizing ulcerative
gingivitis. J Can Dent Assoc 2013;79:d46.
14. 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.
15. 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.
16. 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.
17. Slots J. Herpes viral‑bacterial interactions in periodontal diseases.
Periodontol 2000 2009;51:1‑24.
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