Infectious Diseases of Oral Cavity

ARTICLE IN PRESS
JID: YMDA [mUS1Ga;October 26, 2018;19:56]

Disease-a-Month xxx (xxxx) xxx
Contents lists available at ScienceDirect
Disease-a-Month
journal homepage: www.elsevier.com/locate/disamonth
Infectious diseases of oral cavityR

Shailesh Gondivkar a, Amol Gadbail b, Gargi S. Sarode c,
Sachin C. Sarode c,∗, Shankargouda Patil d, Kamran H. Awan e
a
Department of Oral Medicine and Radiology, Government Dental College & Hospital, Nagpur, Maharashtra, India
b
Department of Dentistry, Indira Gandhi Government Medical College and Hospital, Nagpur, Maharashtra, India
c
Department of Oral Pathology and Microbiology, Dr. D. Y. Patil Dental College and Hospital, Dr. D.Y. Patil
Vidyapeeth, Sant-Tukaram nagar, Pimpri, Pune 411018, Maharashtra, India
d
Department of Maxillofacial Surgery and Diagnostic Sciences, Division of Oral Pathology, College of Dentistry,
Jazan University, Jazan, Saudi Arabia
e
College of Dental Medicine, Roseman University of Health Sciences, South Jordan, UT 84095, United States
Contents
Viral infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
Herpes simplex virus infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Differential diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Herpes zoster virus infection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Herpangina . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Hand-foot-and-mouth disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
HIV disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Infectious mononucleosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
R
Conflict of interest statement: The authors have no conflicts of interest in relation to the present work.
∗
Corresponding author.
E-mail address: sachin.sarode@dpu.edu.in (S.C. Sarode).
https://doi.org/10.1016/j.disamonth.2018.09.008
0011-5029/© 2018 Published by Elsevier Inc.
Please cite this article as: S. Gondivkar et al., Infectious diseases of oral cavity, Disease-a-Month (2018),
ARTICLE IN PRESS
2 S. Gondivkar et al. / Disease-a-Month 000 (2018) 1–21
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 8

Differential diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 8
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 8
Human papillomavirus-associated oral lesions . . . . . . . . . . . . ... . .. . ... ... . ... ... . 8
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 8
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 8
Mumps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 9
Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 9
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 9
Involvement of viral factors with head and neck cancers . . . . ... . .. . ... ... . ... ... . 9
Bacterial infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 9
Tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 10
Leprosy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 11
Actinomycosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 12
Syphilis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 13
Syphilitic leukoplakia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 13
Congenital syphilis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 13
Gonococcal stomatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 14
Fungal infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 14
Superficial oral fungal infections. . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 14
Group 1: Candidial lesions confined to oral and perioral areas . . . ... . .. . ... ... . ... ... . 14
Pseudomembranous candidiasis . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 14
Erythematous candidiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 15
Plaque-like candidiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 15
Denture stomatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 15
Angular cheilitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 16
Central papillary atrophy (median rhomboid glossitis) . . . . . . ... . .. . ... ... . ... ... . 16
Deep-seated oral fungal infections . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 16
Aspergillosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 16
Blastomycosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 17
Histoplasmosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 17
Coccidioidomycosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 17
Paracoccidioidomycosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 17
Crytpococcosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 17
Mucormycosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 17
Diagnosis of oral fungal infections . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 17
Treatment of oral fungal infections . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 18
Azoles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 18
Polyenes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 18
Echinocandins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 18
Pyrimidines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 18
Declarations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 18
Competing interests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 18
Funding statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 19
Author’s contribution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 19
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 19
Viral infections
Patients with viral infections of the over cavity can pose a challenge to clinicians. Pri-
mary and secondary or recurrent lesions of the viral infections can be extremely painful and
debilitating. The most common among the viral lesions presenting with oral manifestations is
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S. Gondivkar et al. / Disease-a-Month 000 (2018) 1–21 3
herpes simplex virus (HSV) infection. Less common is the varicella zoster virus (HZV) infec-
tion. Other viral infections include herpangina, hand-foot-and-mouth disease, mumps, infectious
mononucleosis, human papillomavirus-associated oral lesions and HIV-AIDS. Primary care physi-
cian play a crucial role in the diagnosis and management of these conditions.
Herpes simplex virus infection
Description
Humans are the only natural reservoir of HSV infection. HSV infections spread by direct in-
timate contact with lesions or secretions from an asymptomatic carrier.1 Oral infections with
HSV occur in two clinical forms: primary herpetic gingivostomatitis and secondary lesions of
recurrent herpes.
Primary HSV infections usually occurs in children and teenagers or in adults without prior
history of exposure to HSV.2 The onset of primary herpetic gingivostomatitis is abrupt and
often accompanied by prodromal features including fever, chills, malaise, headache, nausea,
anorexia, irritability for 1–2 days. This is followed initially by generalized acute marginal gin-
givitis with inflamed and edematous gingiva. In adults, sore throat and tonsillitis are typically
more common than in children. Numerous small, thin-walled vesicles then appear over the af-
fected oral mucosa, which breaks quickly and are seldom seen by clinicians. After they rup-
ture, the lesions appear as small shallow round ulcers, which are covered by yellow fibrin
on all portions of the oral mucosa. Both the movable and attached oral mucosa can be af-
fected. Adults often have ulcerative lesions on their tonsil and posterior pharynx and less fre-
quently on the oral mucosa. As the disease progresses, the adjacent small ulcers may coalesce
to form larger, irregular ulcers and the lesions begin healing in a week to 10 days. HSV may
continue to be present in the saliva for up to a month after the onset of disease. The pri-
mary generalized infection is often accompanied by cervical lymphadenitis and an inability to
eat or drink. Herpetic whitlow is a HSV infection involving one or more finger, which occurs
when virus following the inoculation of virus from an active lesion or infected secretions to
the broken skin thus infecting the epithelial layer. Following this, the virus replicates and forms
vesicles on the finger.3 Healthcare workers can be infected if they examine a patient without
gloves.
Few patients suffer from recurrent intraoral herpes. Recurrences are thought to be triggered
by exposure to sunlight or cold, febrile diseases, stress, trauma, and immunosuppression.4 Re-
current intraoral herpes infections presents as small ulcers preceded by vesicles and commonly
appear on the hard palate. Recurrent herpetic labialis (RHL) also known as fever blisters or cold
sores, is a recurrent HSV infection which occurs on the lips. These lesions typically present as
a cluster of small vesicles on the lips. The vesicles rupture in 1–2 days to form small ulcers of
1–3 mm that spontaneously heal without scarring within 6–10 days. Prodromal symptoms usu-
ally precede the eruptions in the form of tingling or burning. Maximal viral shedding occurs
within the first 24 hours but may last for 5 days.
Differential diagnosis
The differential diagnosis for the lesions of the primary herpetic gingivostomatitis includes
erythema multiforme, apthous ulcers, herpangina, and hand-foot-and-mouth disease. Cytology,
viral culture and antibody titer can be helpful for diagnosis. Recurrent intraoral herpes may re-
semble lesions of the herpes zoster and pemphigus vulgaris.
Management
Milder cases are managed by routine supportive measures including fluid maintenance, an-
tipyretics for fever and topical anesthetics prior to meals to reduce pain associated with swal-
lowing. Topical antiviral drugs such as acyclovir can manage RHL. Immunocompromised patients
usually require systemic antiviral medications along with supportive care.
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Herpes zoster virus infection
Description
Herpes zoster virus (VZV) is a herpes virus and can cause both primary and recurrent infec-
tions. Herpes zoster (HZ), also known as shingles is an acute viral disease caused by reactivation
of a latent VZV. Unlike infection with HSV, HZ disease commonly affects older individuals the in-
cidence of HZ increases with age and immunosuppression.5 Characteristically, the lesions of the
HZ appear along the course of the involved nerve. The nerves most commonly involved with HZ
are C3, T5, L1, L2 and ophthalmic branch of the trigeminal nerve. HZ infection affects trigeminal
nerve in a small percentage of patients and oral manifestations may be seen when the maxil-
lary or mandibular division of trigeminal nerve is involved. HZ has a prodromal period of 2–4
days, when a burning sensation, shooting pain or tenderness may appear along the course of
the affected nerve. Oral HZ manifests as a unilateral cluster of vesicles that rupture in 2–3 days,
leaving ulcers surrounded by an erythematous zone. The ulcers heal within 2–3 weeks. Usually
the oral lesions are accompanied by facial lesions along the specific branch of the trigeminal
nerve. Dental pathologies encountered in HZ infection includes pulp necrosis and internal root
resorption of the tooth.6–7 In immunocompromised patients, larger chronic HZ lesions can lead
to necrosis of the underlying bone and exfoliation of teeth.8 Ramsay Hunt syndrome, or HZ
infection of the geniculate ganglion of the facial nerve is manifested as Bell’s palsy, unilateral
vesicles of the external ear and vesicles of the oral mucosa.9 Post- herpetic neuralgia (PHN) is
the most distressing consequence of the oral HZ. The incidence of PHN significantly increases
after the age of 60 years.
Presence of isolated oral lesions without facial eruptions can be confused with herpetic stom-
atitis, herpetiform ulcers and erythema multiforme. Routine cytology, viral culture and evalua-
tion of serum antibody titer can be helpful for diagnosis.
Management
Acyclovir is routinely used for treatment of HZ. Analgesics and sedatives may help to con-
trol pain. Concomitant use of intralesional steroids with topical anesthetics has been advocated
to prevent PHN. Other treatments of PHN include topical capsaincin, tricyclic antidepressants,
gabapentin10 and chemical or surgical neurolysis in refractory cases.
Herpangina
Description
Herpangina (HA) is a common infectious disease usually caused by coxsackie-virus (CV)
group A, types 1–6, 8, 10, 22.. Unlike HSV infection, HA occurs in epidemics, with highest in-
cidence during summer and autumn. In many countries, epidemics occur every 2–3 years and
primarily affects children, although it may occur in any age group. The disease begins with fever,
sore throat, dysphagia and malaise. Eventually, eruptions appear in the form of macules which
evolve into papules and vesicles within 24–48 hours. The numerous small vesicles break quickly
to form shallow ulcers. The common sites involved by HA are posterior part of oral cavity in-
volving posterior pharynx, soft palate and uvula, tonsils and faucial pillars.11 The disease heals
without treatment within 7–10 days.
The findings of HA may resemble lesions of the primary herpetic gingivostomatitis, apthous
ulcer, acute lymphonodular pharyngitis and erythema multiforme. The diagnosis usually is based
on clinical presentation. Viral isolation from culture and serologic rising antibody titers can be
used to confirm the diagnosis.
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Management
As HA is self-limiting disease; the therapy is directed towards symptomatic relief including
proper hydration.
Hand-foot-and-mouth disease
Description
Hand-foot-and-mouth disease (HFMD) is usually caused by several serotypes of from human
enterovirus A group, including enterovirus 71 and CV-A16.12 HFMD causes a substantial disease
burden in the Asia-Pacific region particularly in young children below 5 years of age.13 HFMD is
manifests as low grade fever, small oral vesicles which breaks rapidly and forms shallow ulcers
surrounded by red halo. Hard palate, tongue and buccal mucosa are the commonest sites of
involvement.11 As the name describes, oral lesions are accompanied with lesions on the extensor
surfaces of the hands and feet. Most of these lesions usually heals in a week.
The differential diagnosis includes HA, herpetic stomatitis, apthous ulcer.
Management
The therapy for HFMD is directed towards symptomatic relief with supportive care.
HIV disease
Description
The HIV/AIDS represents a pandemic form of immunodeficiency. From 30 to 80 percent of the
affected patients demonstrate HIV related oral abnormalities mainly the result of HIV induced
destruction of CD4 T lymphocytes and immune compromise. In 1993, EC-Clearinghouse on Oral
Problems Related to HIV Infection and WHO Collaborating Centre on Oral Manifestations of the
Immunodeficiency Virus classified oral lesions associated with HIV into three categories: Group
1- Lesions strongly associated with HIV infection, Group 2- Lesions less commonly associated
with HIV infection and Group 3- Lesions seen in HIV infection (Table 1)14 , 15 .
Candidiasis. Oral candidiasis (OC) is the most prevalent oral manifestation and usually associ-
ated with the progression of the HIV disease and is considered a marker of acquired immun-
odeficiency syndrome (AIDS).OC usually present in three different forms: angular cheilitis, ery-
thematous candidiasis, and pseudomembranous candidiasis. Angular cheilitis presents as painful
erythema, fissuring or erosion of the corners of the mouth covered with fine scale.16 Pseu-
domembranous and erythematous candidiasis range from white to red or red/white combina-
tions. The different types of candidiasis may coexist in the same patient. Antifungal medications
like ketoconazole, fluconazole, itraconazole etc. are effective in achieving resolution.
Oral hairy leukoplakia. Oral hairy leukoplakia (OHL) was initially considered as pathognomonic
of HIV infection but has also been encountered with other diseases. OHL is considered to be a
reliable indicator of low CD4 count.17 OHL is caused by Epstein-Barr virus (EBV)18 and presents
clinically as a white non-scrapable corrugated lesion19 most commonly seen on lateral border of
tongue and more prevalent in males.20 Lesions are of rough texture, adherent and asymptomatic.
OHL is most common when CD4 count falls below 200cells/mm3 but can be present at all stages
of AIDS. As asymptomatic, OHL usually does not need treatment. Antiviral therapy (acyclovir) is
useful.
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Table 1
Classification of orofacial lesions associated with HIV/AIDS in adults.
Group 1 Lesions strongly associated with HIV infection

Candidiasis
– Erythematous
– Pseudomembranous
Hairy leukoplakia
Kaposi’s sarcoma
Non Hodgkin’s lymphoma
Periodontal disease
– Linear gingival erythema
– Necrotizing (ulcerative) gingivitis
– Necrotizing (ulcerative) periodontitis
Group 2 Lesions less commonly associated with HIV infection
Bacterial infections
– Mycobacterium aviumintracellulare
– Mycobacterium tuberculosis
Melanotic hyperpigmentation
Necrotizing (ulcerative) stomatitis
Salivary gland disease
– Dry mouth due to decreased salivary flow rate
– Unilateral or bilateral swelling of the major salivary glands
Thrombocytopenic purpura
Ulceration NOS (not otherwise specified)
Viral infections
– Herpes simplex virus
– Human papillomavirus (wart like lesions)
– Condylomaacuminatum
– Focal epithelial hyperplasia
– Verruca vulgaris
– Varicella zoster virus
– Herpes zoster
– Varicella
Group 3 Lesions seen in HIV infection
– Actinomycesisraeli
– E. coli
– Klebsiellapneumoniae
Cat scratch disease
Drug reactions (ulcerative, erythema multiforme, lichenoid, toxic epidermolysis)
Epithelioid (bacillary) angiomatosis
Neurologic disturbances
– Facial palsy
– Trigeminal neuralgia
Fungal infection other than candidiasis
– Cryptococcus neoformans
– Geotrichumcandidum
– Histoplasmacapsulatum
– Mucoraceae (mucormycosis/zygomycosis)
– Aspergillusflavus
Recurrent aphthous stomatitis
Viral infections
– Cytomegalovirus
– Molluscumcontagiosum
Kaposi’s sarcoma. Though HIV infection is associated with different malignant tumors, Kaposi’s
sarcoma (KS), is the most frequently encountered oral malignancy.21 Kaposi’s sarcoma-associated
herpesvirus (KSHV)/ human herpes virus-8 (HHV-8) has been recognized as the causative organ-
ism.22 In the oral cavity, KS presentation ranges from red/purple macule to nodule which can get
ulcerated. Lesions are commonly seeen on the palate and gingiva. Initially, KS lesions are flat,
red, and asymptomatic, with the color becoming darker as the lesion progresses. Lesions of KS
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can grow to a very considerable size and in advanced AIDS are likely to be multiple. Larger le-
sions may be asymptomatic or cause minor symptoms due to irritation and/or ulceration during
speaking or chewing. Treatment for KS consists of low dose radiation therapy and intralesional
or treatment with systemic chemotherapeutic agents.
Non-Hodgkin’s lymphoma. Non-Hodgkin’s lymphoma (NHL) is the second most common malig-
nancy associated with AIDS and is 60 times more prevalent in AIDS patients compared to un-
infected individuals.23 NHL is caused by Epstein Barr Virus (EBV) and majority of lymphomas
are of B cell origin. Intraoral NHL presents as inflammatory growth and ulceration,24 commonly
involving gingiva, followed by hard palate.25
Periodontal diseases. HIV infected patients are vulnerable to periodontal diseases including lin-
ear gingival erythema (LGE), necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative
periodontitis (NUP). LGE usually manifests as fiery red band along the gingival margin in associ-
ation with anterior teeth that may be associated with bleeding and discomfort.16 NUG and NUP
tend to be different stages of the same disease (necrotizing ulcerative disease). Characteristically,
there is rapid destruction of the soft tissues in the NUG and bone in the NUP. NUG presents as
rapid onset and acute painful inflammation of gingiva. NUP is characterized by severe pain, teeth
mobility, bleeding, fetid odor, ulcerated gingival papillae, and rapid loss of bone and soft tissue.
The triggering factors considered for aggravation of NUG and NUP include changes in the im-
mune status, stress, anxiety, malnutrition and smoking. These periodontal diseases merit referral
for dental care and are managed by aggressive dental prophylaxis, debridement, and antibiotic
treatment with metronidazole as the drug of choice. Patients are advised to maintain good oral
hygiene by using chlorhexidine rinses.
Other bacterial infections. This includes primary tuberculosis (TB) of the oral cavity, syphilis and
infections caused by Actinomyces Israelii, Escherichia coli and Klebsiella pneumonia. Intraoral TB
clinically presents as painful granulomatous ulcers on the tongue and palate. Syphilis is charac-
terized by chancre, mucous patches and gummatous ulcerations in the primary, secondary and
tertiary stages of syphilis respectively.
Salivary gland disease. HIV infection can lead to salivary gland enlargement and xerostomia.25
Parotid gland is commonly involved, followed by the submandibular gland. Reduced salivary flow
can result from salivary gland disease and can be aggravated by medications like antiretroviral
agents.
Herpes simplex infection. Recurrent herpetic lesions manifests in the form of vesicles and small,
shallow ulcerations and subsequent healing. Lesions on the lips are common and intraorally the
palate, gingiva and other keratinized mucosa are frequent sites of involvement. Often, oral her-
petic lesions are often self-limiting however, an anti-viral drug like acyclovir is recommended
for fulminating infections.
Herpes zoster infection. Lesions of the HZ result from reactivation of latent VZV in cases of im-
munosuppression. Multiple dermatomes might be involved and the condition is associated with
sever PHN.21 The drug of choice for HZ in HIV positive patients is acyclovir.
Human papilloma virus infections. Human papilloma virus (HPV) infection can present in mul-
tiple forms including verruca vulgaris, focal epithelial hyperplasia and condyloma acuminatum.
Oral warts present as pedunculated or sessile papillomatous growths. The common sites of in-
volvement are palate, buccal mucosa, and labial commissure. Occasionally, condyloma acumina-
tum might develop in orofacial area. Clinically, the lesions are multiple painless, whitish and
cauliflower shaped.
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Cytomegalovirus infection. The lesions associated with cytomegalovirus (CMV) infection are non-
specific ulcerations that can occur anywhere on the oral mucosa. The lesions of CMV infection
are usually only seen in patients having CD4 counts below 100 cells/mm3 .
Management. The treatment of HIV associated oral lesions is symptomatic and topical or sys-
temic or both along with antiretroviral therapy (ART) and highly activated antiretroviral therapy
(HAART).
Infectious mononucleosis
Description
Infectious mononucleosis (IM), commonly referred to as “glandular fever,” is an acute self-
limiting benign disease caused by EBV infection. Evidence of previous exposure is found in ap-
proximately 90% of the world’s adult population.26 Transmission of the virus usually occurs via
saliva by kissing and transmission is more common in young adults. Most infected patients are
asymptomatic with approximately one third patient developing manifestations. IM is character-
ized by a triad of fever, lymphadenopathy and pharyngitis.26 Splenomegaly, hepatomegaly may
occur in few patients. An atypical lymphocytosis supports the diagnosis as does a positive het-
erophile antibody test. The oral manifestations include palatal petechiae, uvular edema, tonsillar
exudate, diffuse erythema of the oral mucosa, gingivitis and rarely ulcerations.
The oral lesions of IM may resemble lesions of streptococcal oropharyngitis, diphtheria, Vin-
cent’s infection, leukemia and drug reactions. The lymphadenopathy caused by proliferation of
mononuclear cells may be confused with malignancies such as lymphoma or from infections
such as TB or HSV.. The diagnosis is confirmed by serology; the presence of heterophile anti-
body is used as a rapid screening test.27
Management
The treatment is mainly supportive. Using amoxicillin or ampicillin in patient with active
infection should be avoided because of the high incidence of rash.
Human papillomavirus-associated oral lesions
Description
The oral lesions associated with HPV include verruca vulgaris, focal epithelial hyperplasia
and condyloma acuminatum. Verruca vulgaris clinically appears as a small, sessile, exophytic
cauliflower-like or spiked surface with a whitish color. These lesions are commonly seen on the
lips and palate. Focal epithelial hyperplasia is characterized by multiple painless, smooth, soft
nodules with a flat base and appears whitish or normal in color which disappears on stretching
the mucosa. Common sites of involvement include the lower lip, followed by buccal mucosa,
tongue, gingiva and palate. Condyloma acuminatum rarely appear in the oral mucosa due to
autoinoculation from genital lesions or during oro-genital contacts. Clinically, it appears as single
or multiple small, sessile cauliflower-like growths with a whitish or normal color. Tongue, lips,
buccal mucosa, gingiva and palate are commonly involved.
Papilloma, fibroma, verrucous carcinoma can present similarly to HPV lesions. Diagnostic
tests include histopathologic examination and DNA hybridization.
Management
Surgical excision is the treatment of choice.
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Mumps
Description
Mumps is an acute viral infection caused by mumps virus (MuV), a member of the family
paramyxoviridae. Humans are the only natural host for MuV. The incubation period is between
16–24 days and transmission of virus may occur via saliva droplets in the air.28 It character-
ized by unilateral or bilateral swelling of the parotid salivary glands. This may be associated
with low-grade fever, chills, headache, and malaise. The characteristic sign of mumps is the ten-
der, rubbery swelling of the parotid glands lasting for about 7 days. Mumps commonly seen
in children and young adolescents. If adults are involved, severe consequences such as orchitis,
oophoritis, hearing loss, pancreatitis and meningo-encephilits may be associated.
Acute supppurative parotitis, sialolith in the salivary glands, Sjogren’s syndrome, salivary
gland neoplasm and lymphadenopathy.
Management
Mumps can be managed by symptomatic treatment with supportive care.
Involvement of viral factors with head and neck cancers
Along with other established risk factors, some viral infections are linked to head and neck
cancers. The viruses associated with cancer transformation include HPV, herpes group viruses,
adenoviruses and hepatitis C viruses. Of these, HPV and herpes viruses are now considered to
be the most likely “synergistic viruses” in human oral cancer.29 Herpes viruses including Epstein
Barr Virus (EBV), Human Herpes virus 8 (HHV-8) and Cytomegalovirus (CMV) often linked to
oral cancer.30,31 the malignancies associated with EBV are nasopharyngeal carcinoma, Burkitt’s
lymphoma, post-transplant lymphoma and gastric carcinoma.32 HHV-8 can results in all forms
of Kaposi’s sarcoma, primary effusion lymphomas and multicentric Castleman’s disease.31 , 33–35
CMV is a common pathogen that infects majority of the population.36 CMV is linked to tumors
such as brain cancer37 and salivary gland cancer.38 Saravani et al. suggested a minor role of CMV
in oral squamous cell carcinoma (OSCC).39 HPV have been categorized by their genotypes into
low-risk and high-risk types according to associated lesion’s propensity for malignant progres-
sion.40 There is a high prevalence of association of HPV, particularly high-risk genotypes (HPV
16 and 18) with OSCC41,42 and oropharyngeal carcinoma.43
Bacterial infections (BI) of the oral cavity are becoming more common worldwide. BI of
oral cavity are usually due to the following factors (a) weakened host resistance resulting in
overgrowth of microorganisms; (b) older adults with systemic diseases; (c) use of immunosup-
pressive drugs; (d) poor oral hygiene maintenance with nutritional deficiencies (e) mechanical
trauma or ulcerations leading to secondary mucosal infections. Impairment of systemic or local
host defenses may results in opportunistic bacterial infections of oral cavity. While less common,
BI can also occur in the oral cavity in healthy individuals. It is very important to distinguish be-
tween non-odontogenic infections and odontogenic infection. The most common odontogenic
infections are dental caries, gingivitis, periodontitis, endodontic infections, dental abscesses and
pericoronitis. Bacteria present in the dental plaque are the most common cause of odonto-
genic infections. While generally not pathogenic, if the bacteria in plaque multiply to high levels
and invade in to deeper tissue they can initiate and maintain an active infectious processes. In
this review, we focused our discussion on the oral manifestations of non-odontogenic systemic
infections.44
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Tuberculosis
Mycobacteria strains are the etiologic agent of Tuberculosis infections (Mycobacterium tu-
berculosis in humans). It is a chronic granulomatous and potentially deadly infectious disease.
Lungs are the most common primary site of involvement although multiple other organs can be
affected by tuberculosis. TB spreads primarily by aerosolizatoin, especially from persons with TB,
who cough, spit or sneeze. Most infections remain asymptomatic and become latent infection in
humans. In humans, around ten percent of latent infections eventually progresses to active dis-
ease. The HIV positive individual carries a 10% annual risk of tuberculosis, compared to a 5%
lifetime risk in HIV negative individual.45
Tuberculosis with oral manifestations is rare, accounting for 0.1%–5% of all TB infections. Oral
manifestations are usually due to hematogenous spread or from secondarily inoculation with
infected sputum.46 The oral lesions are manifested in a variety of forms and can appear any-
where within the oral cavity. However, tuberculous ulcers produce a distinct stellate ulcer with
undermined edges and granulating floor, which is often painful, ragged and not indurated. r.
While lesions can appear anywhere within the oral cavity, the tongue is the most common site
followed by the gingiva, palate, floor of mouth, lips and buccal mucosa.45
Oral TB lesions are classified as either primary or secondary. Primary tuberculous le-
sions are rare and may present as a single painless ulcer with enlargement of regional
lymph node frequently seen in younger patients.47 In contrast, the secondary TB lesions
are more common and usually associated with pulmonary TB. The secondary lesions usu-
ally appear as a single, painful irregular, indurated ulcer covered with inflammatory exu-
dates. The secondary tuberculous lesions can be seen in any age group but more com-
monly affect in middle-aged and elderly patients.48 The tongue is usually the most af-
fected site, but lesions may occur anywhere in the oral cavity. Other sites include the
palate, gingiva, buccal mucosa, floor of the mouth, and lips. TB infections may also f
involve the salivary glands, tonsils, and uvula. The retro-molar region and mandibular
ridge (alveolar mucosa) are rarely involved. The oral tuberculous lesions commonly man-
ifest as either ulcers, nodules, tuberculomas andperiapical granulomas.49 Superficial ulcers,
patches, indurated soft tissue lesions are the most common oral manifestations of TB. TB
can also cause mandibular osteomyelitis which appears on radiograph appear as a sim-
ple bony radiolucency.49 The oral ulcerative tuberculous lesions are often painful with-
out caseation necrosis of the dependent lymph nodes. TB lesions are often overlooked
in the differential diagnosis of oral lesions due to their nonspecific clinical presentation
and while not common should be considered when oral lesions are preceded systemic
symptoms.
An ulcer on the lateral border of the tongue is the commonest site for primary TB le-
sion. This may be facilitated by chronic irritation or inflammation on the lateral border of
tongue due to close proximity to posterior teeth.50 These tongue lesions are symptomatic and
cause severe, continuous and progressive pain that can interfere with proper nutrition and
rest. Tongue lesions are irregular, pale, granulations on the floor with sloughing tissue with
indolent and inverted margins.51 In children and adolescents, primary tuberculous involve-
ment of gingival is more common than adults. The gingival ulcer usually manifests as a sin-
gle painless indolent ulcer, which progressively extends from marginal gingiva to the depths of
vestibule.50
Unusual forms of the TB in the oral cavity are becoming more common due to the increas-
ing prevalence TB. Doctors and dentists should be aware of the oral manifestations of TB and TB
should be considered in the differential diagnosis of suspicious or non-healing oral ulcers. s. Oral
TB lesions mimic malignant lesions and others like actinomycosis, syphilitic ulcer, Wegener’s
granuloma, traumatic ulcers, and apthous ulcers. A traumatic ulcer is acute, of short duration,
exquisitely tender and occurs in areas of chronic irritation.52 Chronic oral tubercular ulcer with
indurations should be carefully differentiated from oral cancer as they both share similar clini-
cal manifestations.53 On histological examination, other entities like sarcoid, cat scratch disease,
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Table 2
Non-specific and specific oral lesions seen in leprosy.58
Leprosy–non-specific lesions Enanthem of palate or uvula
Leprosy-specific lesions Lips Flat-topped nodules

Macrocheilia
Microstomia
Tongue Multiple superficial ulcers
Mild glossitis
Loss of papillae
Fissured tongue
Nodules on anterior tongue
Atrophy
Pavement-like appearance
Buccal mucosa Diffuse infiltration
Papulonodules and ulceration
Pale mucosa
Hard and soft palate Loss of shininess of mucosa
Erythematous papules
Nodular sub-mucosal infiltrate
Palatal ulceration
Palatal perforation
Uvula and fauces Miliary papules and nodules
Triangular deformity of fauces
Dental Gingivitis
Periodontitis
Periodontoclasia
Specific pulpitis
Periapical granulomas
Crohn’s disease, tertiary syphilis, foreign body reaction, and Melkersson Rosenthal syndrome also
demonstrate granulomatous changes.
Laboratory investigations:-Identification of acid fast bacilli in the specimen either by PCR
or acid fast bacilli staining and culture of tuberculosis bacilli confirm the diagnosis of TB.54
Other supportive modes of confirmatory diagnosis are sputum culture, radiographic evidence
and biopsy to rule out systemic TB, Mantoux skin test and chest x-ray are mandatory steps. Use
of standard antitubercular therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for at
least six months is needed for complete remission of tuberculous infection.55
Leprosy
Leprosy is a chronic multi-system infectious disease caused by Mycobacterium leprae.

The presentation of leprosy is determined by the complex interaction between the invading
organism and host immune status. The most commonly involved organs are the skin, peripheral
nervous and monocyte–macrophage systems. However, a mild to moderate degree of infiltra-
tion is seen in other organ systems including the liver, kidneys, eyes, oral mucosa, lymph nodes,
bones and joints and gonads. In the lepromatous form of leprosy, oral lesions are more common
and are typically late manifestation. Oral lesions in lepromatous leprosy as a source of infection
have a great epidemiological importance.56 The oral manifestations of leprosy involves asymp-
tomatic, insidious lesion on the hard palate. Hard palate involvement are usually secondarily
involved from nasal lesions.57 Table 1 enumerates the various non-specific and specific lesions
affecting the oral cavity in leprosy.58 Morphologically the oral lesions manifest in the form of
enanthems to ulcers, perforations and scars, papules and nodules (lepromas). In the oral cavity,
superficial erosions are common with involvement of palate, tongue, uvulae, lips and gingiva.
(Table 2).
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1. Palate: ulceration and perforation are present in middle of palate and extending to soft
palate. Sometimes reddish or yellow-reddish nodules varying from 2–10 mm are also
present.59,60
2. Tongue: lesions on the tongue are seen in 17%–25% of cases. The anterior, dorsal surface is
affected in about two-third of patients with a “paving stone appearance” due to loss of the
papillae and longitudinal fissures, erosions and nodular infiltration.61
3. Uvula: in extreme cases, there may be intense fibrosis or complete destruction of the uvula.60
4. Lips: there may be macrocheilia or microstomia and subsequent repair with fibrosis leads to
perioral or lip lepromas.60
5. Gums: palatal gingival in upper anterior region are usually affected. Chronic gingivitis, peri-
odontitis and periodontoclasia may occur.62
6. Atrophy of nasal spine and pre-maxillary processes subsequently result in loss of the upper
incisors. These facial changes are termed as facies leprosy.63
Oral involvement is based on the fact that Mycobacterium leprae favors and multiplies at tem-
peratures a little below the body temperature. In lepromatous leprosy, oral breathing is common
because of air flow obstruction due to nasal lesions and causes decrease in the intra-oral tem-
perature facilitating the harboring of the bacillus inanterior areas.64 The sequence of patholog-
ical changes in the nasal and oral mucous membranes are: congestion and infiltration leads to
nodules formation, followed by ulceration, atrophy and finally fibrosis.65 In the advanced stages,
deformities and functional alterations such as serious disturbances in phonation, and nasal re-
gurgitation of food due to fibrosis and retraction of the soft palate and or perforation of the hard
palate leads to destruction, perforation and deformation.66
Actinomycosis
Actinomycosis is a rare, chronic disease caused by anaerobic Gram-positive bacteria. Humans

are the natural reservoir for bacteria and colonize the mouth, colon, and urogenital tract.67 Acti-
nomyces israelii is the principle causative microorganism for cervicofacial actinomycosis. Rarely
other strains such as naeslundii, viscosus, and odontolyticus are the causative agents.. Actino-
myces israelii causes a gradually developing chronic infection, particularly when the normal pro-
tective mucosal wall is disrupted due to trauma, surgery, or preceding infection.68
The head and neck region accounts for approximately 55% of actinomycosis cases; the
mandible is the most common location. Actinomycosis of the jaws esults in abscess formation
and subsequent open draining sinuses. Actinomycosis may form part of the normal oropha-
ryngeal flora. Disruption of the mucosal barrier is the main triggering factor of the infection
is characterized by chronic sulfur granules, suppurative and granulomatous inflammation that
may result in multiple abscesses and sinus tract formations The clinical presentation may be
either acute or chronic. The acute infection occurs less frequently and may exhibit a fluctuant
swelling, pain and fever. Chronic infection is more common and may evince slowly progres-
sive swelling, with or without symptoms, slight temperature elevation developing over a long
period of time.69 Infections may invade surrounding tissues and to form masses, mimiingc ma-
lignancy.70
Cervicofacial actinomycosis is the most frequent type infection and intraoral localized lesions
occur seldomly.Early in the disease an actinomycosis infection may be misdiagnosed as a pyo-
genic abscess or as malignant lesion leading to inadequate treatment.71 Clinically, actinomycosis
is asymptomatic at any or in later stages.72 However, any unidentified mass, facial swelling, or
persistent infection following endodontic or other relevant treatment should raise the possibil-
ity of actinomycosis.73 Persistent oral infections can lead to serious consequences, especially in
maxilla. Early diagnoses and treatment improve the outcome significantly.74
Penicillin is the drug of choice and should be continued for at least 6 months. Generally,
serious infection and bulky disease should initially be treated with intravenous penicillin for
2–6 weeks followed by oral penicillin for 12 months, Milder disease can be treated with oral
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agents for a shorter period.75 In patients allergic to penicillin, tetracycline, erythromycin and
clindamycin are reasonable alternatives.76 Relapse is a common feature of the disease; thus long-
term follow up of the patient is mandatory.
Syphilis
Treponema pallidum, an anaerobic tightly coiled helical bacterial species, causes syphilis.
Direct transmission can be vertical (congenital syphilis) or sexual (acquired syphilis). However,
indirect transmission may result from contaminated objects.77 Syphilis has three clinical stages.
The primary stage syphilis occurs about 90 days after exposure and remits spontaneously within
2–8 weeks. It is characterized by appearance of a single chancre. The secondary stage may be-
come evident between 2 and 12 weeks after exposure and is characterized by a skin rash and
subsides spontaneously without any treatment and followed by a latent stage. The tertiary stage
or late stage syphillis is rarely observed today and starts 3 years or later after exposure. It is
characterized by gummata and/or neurosyphilis.78,79 Oral manifestations of syphilis are mostly
noted at the secondary stage of syphilis, however can be seen in the primary stage. Oral lesions
manifests as multiple painless irregularly shaped or apthous like ulcers with whitish edges on
the tongue, lips, and lingual mucosa and oropharynx.79 Mucous patches are the most common
oral sign of secondary syphilis. Mucous patches consist of two subtypes. (a) Slightly elevated oval
plaques and sulcerated lesions covered with a gray or white pseudomembrane. Multiple mucous
patches may coalesce to form serpiginous lesions called as snail track ulcers. (b) Leukoplakia like
are white plaques with a verrucous aspect. However, syphilis varies in presentation and atypical
cases may result in delayed or missed diagnosis.80,81 Patient may complain of sore throat due to
the diffuse inflammation of oropharynx. In contrast to primary syphilis, the oral manifestations
of secondary syphilis are not associated with oral sex habits.79 Medical and dental practition-
ers should consider ulcerative lesions of secondary syphilis in the differential diagnosis of other
white and ulcerative oral lesions, particularly in sexual active group.82
Syphilitic leukoplakia
Syphilitic leukoplakia may appear as a homogenous white patch on the dorsum of tongue
involving large areas. The literature suggests oral squamous cell carcinoma, particularly of the
tongue, may develop in tertiary stage of syphilis. However, the risk of malignant transformation
of syphilitic leukoplakia in syphilis remains unclear due to (a) a direct consequence of infection
(which seems unlikely) or (b) is the effect of recognized etiological factors for oral malignancy
such as tobacco, alcohol, and malnourishment.83
Congenital syphilis
Only after the 16th week of intrauterine life can Treponema pallidum cross the placenta.
Hence, the effect on facial structures varies depending upon the time of infection. The orofa-
cial manifestations of congenital syphilis can be categorized into early and late. Early features
of orofacial manifestations of congenital syphilis include diffuse maculopapular rash, periosti-
tis (frontal bossing of Parrot), and rhinitis. Late features of congenital syphilis usually develop
at least 24 months after birth. Hutchinson’s triad, seen in late features, consists of intersti-
tial keratitis of the cornea, sensorineural hearing loss, and dental anomalies. The permanent
incisors and first molars are typically affected and usually the maxillary incisors in congeni-
tal syphilis because tooth calcification occurs during the first year of life. The affected incisors
have a screwdriver shape and the crown of lateral incisors appears convergence towards the in-
cisal edge. Eventually (Parrot’s) radial scars rhagades of the lips are appear. The characteristics
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well-circumscribed border of the vermillion may disappear. Atrophic glossitis and a high narrow
palatal vault are other rare orofacial features. Facial neuropathies may also rarely occur.84
Penicillin is drug of choice for treating syphilis s and both penicillin G benzathine or peni-
cillin G procaine are effective.77 For penicillin allergic patientspenicilli doxycycline or tetracy-
cline, or azithromacin are effective alternatives.85
Gonococcal stomatitis
Neisseria gonorhoeae rarely gives rise to gonococcal stomatitis. Gonococcal stomatitis is usu-
ally transmitted through the orogenital sex (fellatio, cunnilingus) and thus more commonly ob-
served in women and homosexual men. The oral lesion of gonococcal stomatitis appears as
atypical fiery erythema and sometimes superficial ulcer formation covered with a grayish or
yellowish-exudate. The common symptoms are burning sensation, mild pain and sore throat.
The most common sites of involvement are the pharyngeal area, uvula, soft palate and tonsils.
The tongue, buccal mucosa, and gingiva are rarely affected by gonococcal stomatitis. If clinical
features suggest gonococcal stomatitis, identification of the microorganism should be done to
confirm the diagnosis. Differential diagnosis includes herpetic stomatitis, streptococcal stomati-
tis, erythematous candidiasis, mechanical trauma and thermal burn.
The oral lesions are frequently self-limited. Oral administrations of penicillin or tetracyclines
are the drugs of choice. Avoid elective dental procedures if possible in patients with active gon-
orrhea with oral lesions.86
Fungal infection
The recognition that fungi causes disease dates back to around 4th century when Hip-
pocrates, the Father of Medicine, first described fungal infectionsin humans.87 Since then several
clinical variants of fungal diseases have been recognized. For ease of understanding the etiology
and management, human fungal infections can be broadly categorized into superficial oral fungal
infections and deep-seated oral fungal infections.
Superficial oral fungal infections
Oral candidiasis, is the most commonly encountered superficial oral fungal infection. Most
clinically reported cases of oral candidiasis, around 70%−80%, are caused by Candidia albicans, an
obligate organism found in the digestive tract and vaginal tract of humans. Other non-candida
albicans species like C. glabrata and C.tropicalis accounts for around 5% and 8% of the reported
cases respectively.88 These species cause disease through direct tissue invasion, inducing a hy-
persensitive state or by producing potent Candida toxins.89 Conditions in the host such as re-
duced salivary flow, use of broad-spectrum antibiotics, deficiency of certain nutrients, denture
wearing, diseases and drugs causing immunosuppression fosters the growth of Candida and pro-
motes oral candidiasis.90 Many attempts have been made to classify this disease that comes in
a variety of clinical forms. The most recent classification groups candidiasis into two major cat-
egories: Group 1 (primary oral lesions) and Group 2 (secondary lesions).91 See Table 3.
Group 1: Candidial lesions confined to oral and perioral areas
Pseudomembranous candidiasis
Langenbeck in 1839 first described a pseudomembranous variant of candidiasis, now com-

monly referred to as oral thrush, in buccal aphthae in a typhus patient.88 Clinically, it may ap-
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Table 3
Classification of oral candidiasis.
Group 1: Candidal lesions that are confined to oral and perioral areas only
Sub-group 1: acute variants
Pseudomembranous
Erythematous
Subgroup 2: chronic variants
Pseudomembranous
Erythematous
Plaque-like
Sub-group 3: Candida associated lesions
Denture stomatitis
Central papillary atrophy
Angular cheilitis
Group 2: Oral candidial lesions accompanied by systemic mucocutaneous manifestations
Familial chronic mucocutaneous candidiasis
Diffuse chronic mucocutaneous candidiasis
Candidiasis endocrynopathy syndrome
Familial mucocutanoeus candidiasis
Severe combined immunodeficiency
DiGeorge syndrome
Chronic granulomatous disease
Acquired immunodeficiency syndrome (AIDS)
pear as white or yellow plaques that frequently resembles cottage cheese or curdled milk on the
affected mucosal surface. The plaque constists of a fungal overgrowth causing epithelial desqua-
mation and a resultant accumulation of bacteria and necrotic and keratineceous tissue. The le-
sion can be diffuse or discrete and is easily removed with gauze, causing bleeding and leaving
a raw area underneath. It can be acute or chronic in nature. Thrush is most commonly seen
in individuals with disturbed immune-system such as infants and elderly, patients with severe
immunosuppressive diseases or those taking medicines that suppresses immunity.
Erythematous candidiasis
Previously referred to as atrophic candidiasis, erythematous candidiasis typically presents

as areas of erythema on oral mucosal surface. Many experts consider it to be a successor of
pseudomembranous candidiasis. It has diffuse red borders that help to distinguish it from other
mucosal lesions, especially erythroplakia. It can be acute or chronic and most often affects the
palate and dorsum of the tongue causing depapillation. Erythematous type of candidiasis usually
affects individuals using broad-spectrum antibiotics or steroids.
Plaque-like candidiasis
Chronic plaque-like candidiasis replaces the former term called chronic hyperplastic candidi-
asis or candidial leukoplakia. It represents a white patch on the affected oral mucosal surface
that cannot be easily scrapped off. It is the least common variant and has a considerable po-
tential for malignant transformation. Even though the exact role of yeasts in malignancy is not
known, it is hypothesized that they catalyze nitrosamine production.91
Denture stomatitis
Denture stomatitis or denture sore mouth, as it is commonly referred to, is a chronic inflam-
mation of denture bearing palatal mucosa caused by microbial flora, including C. albicans. The
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porosities within the acrylic denture supports fungal and bacterial accumulation and growth re-
sulting in areas of inflammatory changes. The area under the denture provides C. albicans and
other bacterias like Streptococcus-, Veillonella-, Lactobacillus-, Prevotella-, and Actinomyces-strains,
an anaerobic environment and shields from the flushing action of the saliva.5 Based on their
clinical presentation, Newton classified denture stomatitis into 3 clinical types: Type 1 (local-
ized): simple infection with pinpoint hyperemia and is usually traumatically induced. Type 2
(erythematous): covers the entire or a part of the denture covering area. Type 3 (granular): in-
volving the central part of hard palate and alveolar ridge.92
Angular cheilitis
Angular cheilitis an oral candidial infection involving either or both the commissures of the
mouth. It is a mixed microbial infection caused by Candida albicans and Staphylococcus aureus.93
Associated predisposing factors include vitamin B12 deficiency, iron deficiency, facial wrinkling
along the nasolabial folds and reduced occlusal vertical dimension.94 , 95
Central papillary atrophy (median rhomboid glossitis)
Central papillary atrophy is a relatively uncommon condition of oral mucosa which appears
as a rhomboid-shaped hypertrophic or atrophic plaque on the dorsal surface of the tongue.
Though previously assumed to be a developmental defect of the tongue, recent investigations
note a consistent relationship between the lesion and C. albicans. A few patients report similar
mucosal candidial infection involving the soft and hard palate and such a clinical presentation
is termed chronic multifocal candidiasis. When the tongue is at rest, the dorsal tongue lesion
contacts with the palate giving rise to what is commonly referred to as “kissing lesion” with
appearance of similar erythematous lesion on the palate.96
Deep-seated oral fungal infections
Deep-seated fungal infections are very uncommon in oral and peri–oral region. These infec-
tions are commonly associated with individuals who are immunosuppressed such as those with
HIV infection or some malignancies. Some of the reported deep fungal infections in oral cavity
are discussed below:
Aspergillosis
Aspergillosis is the second most common mycostic infection affecting humans after Can-
didiasis, with Aspergillus fumigatus being the most common pathogen. However, A. flavus, A.
glaucus, A. nidulans, A. terreus, A. repens, A. parasiticus and A. niger are other commonly en-
countered forms. It usually affects patient with immunosuppresion causing allergic bronchopul-
monary aspergillosis. When it occurs within oro-facial region it causes antral aspergilloma, indo-
lent chronic sinusitis, allergic sinusitis and invasive aspergillosis of the antrum. It can progress
to the underlying soft tissue and bone resulting in palatal and oral lesions. Oral lesions typically
presents as yellow or black, necrotic ulcers, involving palate or the posterior tongue.97
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Blastomycosis
Blastomycosis is a mycotic infection caused by Blastomyces dermatitidis, a dimorphic fungus.

Cutaneous blstomycosis may extend to lips, or disseminate to produce ulcerating lesions of the
oral mucosa.98
Histoplasmosis
Histoplasomis is an infection caused by H. capsulatum. It usually causes an acute or chronic

respiratory infection or a chronic mucocutaneous disease. Oral lesions commonly present as
an ulcerative or erosive lesions on the tongue, palate or buccal mucosa. Occasionally, isolated
lesions have been reported in apparently healthy persons having no systemic signs of this
disease.99
Coccidioidomycosis
Coccidioides immitis is a pathogen that is associated with coccidioidomycosis which is present

in soil. Systemic infection usually presents as acute pulmonary disease (San Joaquin valley fever)
or at times with erythema nodosum or erythema multiforme. Very rarely the infection may
involve oral cavity where the lesion is typically a verrucous lesion with or without infection of
the underlying jaw.100
Paracoccidioidomycosis
Also referred as South American blastomycosis or Lutz’ disease, paracoccidioidomycosis is

caused by P. brasiliensis. Chronic pulmonary disease is common in paracoccidioidomycosis which
is often encountered with other lesions, especially oral ulcers that are chronic and exophytic.101
Crytpococcosis
Cryptococcosis is a mycostic infection chiefly involving lungs that is caused by Cryptococcus

neoformans, a ubiquitous yeast. Skin of the face, neck and scalp are the common sites for cuta-
neous involvement. Though extremely rare, oral lesions are reported in individuals with HIV
that can present as a non-healing extraction wounds or chronic ulcers on any oral mucosal
surface.102 , 103
Mucormycosis
Mucormycosis is an acute opportunistic infection caused by a saprophytic fungus. It is re-

ported in immunosuppressed individuals with solid organ transplant or poorly controlled dia-
betes. Oral involvement is very uncommon and is usually secondary to nasal or paranasal sinus
infection. Oral lesions present as palatal necrosis or ulceration. The disease can extend to involve
adjacent structures and cause extreme tissue necrosis and may even dissipate to brain.104
Diagnosis of oral fungal infections
Owing to their characteristic clinical presentation, superficial candidial diseases are usu-
ally diagnosed based on the clinical findings. However objective confirmation can be obtained
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through swab culture, exfoliative cytology, salivary assays, imprint culture, and mucosal biopsy.
Even though exfoliative cytology and biopsy can be used to qualitatively determine the presence
of oral Candidiasis, these methods are less sensitive when compared with culture methods.105
Biopsy of suspicious lesions is recommended to detect the deep-seated fungal diseases of oral
mucosa. Recent advances in the detection of invasive fungal infections through development of
sensitive assays enable quick and early detection of the disease. Positive blood culture, detec-
tion of fungal DNA and antigens are some novel methods for diagnosing invasive fungal infec-
tions. Non-culture methods include PCR, galactomannan antigenemia and Western-Blot analysis
to detect antibodies. Moreover, detection of fungal metabolites like D-arabinitol, and 1, 3-beta-
D-glucan can also be useful for establishing r the diagnosis.106
Treatment of oral fungal infections

Patients with fungal infections should be thoroughly examined for any underlying medical
conditions that can predispose an individual to the development of mycotic infections. Most
fungal infections can be managed symptomatically through topical or systemic medications.
Four most commonly used antifungal agents for oral fungal infections are: azoles, polyenes,
echinocandins, and pyrimidines.
Azoles
Azole agents act by inhibiting ergosterol, a main constituent in the cell membrane of fungi
that results in disruption of the fungal cell membrane. Azole antifungals can be subdivided into
2 classes: imidazoles and triazoles. The imidazole group contains clotrimazole, miconazole, and
ketoconazole. Clotrimazole is mainly used for treating erythematous and pseudomembranous
variants of oral candidiasis while miconazole and ketoconazole are used for managing deep-
seated fungal infections. Triazole group contains voriconazole, fluconazole, posaconazole and
itraconazole. Because of their high solubility and specificity for fungal enzymes, triazoles are
less toxic in nature. They are employed for treating oropharyngeal and esophageal candidiasis
and certain systemic fungal diseases including aspergillosis, histoplasmois and blastomycosis.
Polyenes
Polyene agents are fungicidal in nature due to their ability to bind to ergosterol that results
in loss of membrane-selective permeability and leakage of fungal cell contents. Polyene antifun-
gal agents include amphotericin B and its various formulations, and nystatin. Amhptericin B is
primarily used to treat deep-seated fungal infections while nystatin is used to treat localized
oral candidial infections.
Echinocandins
These are separate class of antifungal drugs that include caspofungin, micafungin and anidu-
lafungin. They interfere in fungal cell wall synthesis and are used to treat mycotic infections by
Candida and Aspergillus species.
Pyrimidines
Pyrimidines replaces uracil in fungal RNA with 5-fluorouracil thus inhibiting fungal protein
synthesis. Flucytosine is a pyrimidine antifungal agent that has activity against Candida, As-
pergillus and Cryptococcus strains and is usually used as an adjunct to other antifungal agents
like amphotericin B, fluconazole, or itraconazole.107 , 108
Declarations
Competing interests
The authors did not receive any financial assistance from or have any personal relationships
with other people or organizations that could inappropriately influence (bias) their work.
ARTICLE IN PRESS
Funding statement
None.
Author’s contribution
All authors: concept, design, analyses, interpretation of data, drafting of manuscript or revis-
ing it critically for important intellectual content.
References
1. Nahmias AJ, Roizman B. Infection with herpes simplex viruses 1 and 2. N Engl J Med. 1973;289:781–789.
2. Regezi JA, Sciubba J. Oral pathology: Clinical-Pathological Correlations. Edn. 2. Philadelphia: W.B. Saunders Co.;
1993:1–33.
3. Wu IB, Schwartz RA. Herpetic whitlow. Pediatr Dermatol. 2007;79:193–196.
4. Halford WP, Gebhardt BM, Carr DJ. Mechanisms of herpes simplex virus type 1 reactivation. J Virol.
1996;70:5051–5060.
5. Morgan R, King D. Shingles: a review of diagnosis and management. Hosp Med. 1998;59:770–776.
6. Solomon CS, Coffiner MO, Chalfin HE. Herpes zoster revisited: Implicated in root resorption. J Endod.
1986;12:210–213.
7. Solomon CS, Coffiner MO, Chalfin HE. Herpes zoster revisited: implicated in root resorption. J Endod. 1986;12:210.
8. Schwartz O, Kvorning SA. Tooth exfoliation, osteonecrosis of the jaw and neuralgia following herpes zoster of the
trigeminal nerve. Int J Oral Surg. 1982;11:364.
9. Lynch MA, Brightman VJ, Greenberg MS. Burket’s Oral Medicine, ed. 9. Philadelphia: Lippincott Williams and
Wilkins;1997:11–50.
10. Robotham M, Harden N, Stacey B, et al. Gabapentin for the treatment of postherpetic neuralgia: a randomized
controlled trial. J Am Med Assoc. 1998;280:1837–1842.
11. Pindborg JJ. Atlas of Diseases of the Oral Mucosa. ed 5. Copenhagen: Munksgaard; 1991.
12. Xing W, Liao Q, Viboud C, Zhang J, Sun J, Wu JT, et al. hand, foot and mouth disease in China, 2008-12: An epi-
demiological study. Lancet Infect Dis. 2014;14(4):308–318.
13. Solomon T, Lewthwaite P, Perera D, Cardosa MJ, McMinn P, Ooi MH. Virology, epidemiology, pathogenesis, and
control of enterovirus 71. Lancet Infect Dis. 2010;10(11):778–790.
14. Reznik DA. Oral manifestations of HIV disease. Top HIV Med. 2006;13(5):143–148.
15. Classification and diagnostic criteria for oral lesions in HIV infection. EC-Clearinghouse on Oral Problems Related to
HIV Infection and WHO Collaborating Centre on Oral Manifestations of the Immunodefi ciency Virus. J Oral Pathol
Med. 1993;22(7):289–291.
16. Rimkuviene J. Precancerous and other oral lesions. Vilnius: Progretus; 2003:106–115.
17. Ramirez-Amador V, Ponce-de-Leon S, Anaya-Saavedra G, Crabtree Ramírez B, Sierra-Madero J. Oral lesions as clinical
markers of highly active antiretroviral therapy failure:a nested case-control study in Mexico City. Clin Infect Dis.
2007;45:925–932.
18. Nokta M. Oral manifestations associated with HIV infection. Curr HIV/AIDS Rep. 2008;5(1):5–12.
19. Johnson NW. The mouth in HIV/AIDS: markers of disease status and management challenges for the dental profes-
sion. Aust Dent J. 2010;55(Suppl 1):85–102.
20. Dongo M, Goncalves LS, Ferreira SM, Noce CW, Dias EP, Júnior AS. Gender differences in oral manifestations among
HIV-infected Brazilian adults. Int Dent J. 2013;63(4):189–195.
21. Petersen PE. Policy for prevention of oral manifestations in HIV/AIDS: the approach of the WHO. Global Oral Health
Program. Adv Dent Res. 2006;19:17–20.
22. Bajpai S, Pazare AR. Oral manifestations of HIV. Contemp Clin Dent. 2010;1(1):1–5.
23. Patil K, Mahima VG, Srikanth HS. Extranodal non-Hodgkin’s lymphoma of the gingiva in an HIV seropositive patient.
Indian J Sex Transm Dis. 2010;31(2):112–115.
24. Rimkuvienė J. Precancerous and other oral lesions. Vilnius: Progretus; 2003:106–115.
25. Nokta M. Oral manifestations associated with HIV infection. Curr HIV/AIDS Rep. 2008;5(1):5–12.
26. Cohen JI. Epstein-Barr virus infection. N Engl J Med. 20 0 0;343:481–492.
27. Macsween KF, Crawford DH. Epstein-Barr virus-Recent advances. Lancet Infect Dis. 2003;3:131–140.
28. Centers for Disease Control and Prevention (CDC). Increased Transmission and Outbreaks of Measles ̶ European
Region, 2011. Weekly. 2011;60(47):1605–1610.
29. Gondivkar SM, Parikh RV, Gadbail AR, Solanke V, Chole R, Mankar M, et al. Involvement of viral factors with head
and neck cancers. Oral Oncol. 2012;48:195–199.
30. Park NH, Byung MM, Sheng LL. Role of Viruses in Oral Carcinogenesis. Bethesda,MD: US Department of health and
human services, Public Health Service. National Institutes of Health; 1992 NIH publication No. 92-3461.
31. Chang Y, Cesarman E, Pessin MS, Lee F, Culpepper J, Knowles DM. Identification of herpesvirus-like DNA sequences
in AIDS-associated Kaposi’s sarcoma. Science. 1994;266:1865–1869.
32. Parkin DM. The global health burden of infection-associated cancers in the year2002. Int J Cancer.
2006;118:3030–3044.
ARTICLE IN PRESS
33. Russo JJ, Bohenzky RA, Chien MC, Chen J, Yan M, Maddalena D. Nucleotidesequence of the Kaposi sarcoma-associ-
ated herpesvirus (HHV8). Proc Natl AcadSci USA. 1996;93:14862–14867.
34. Ablashi DV, Chatlynne LG, Whitman Jr JE, Cesarman E. Spectrum of Kaposi’ssarcoma-associated herpesvirus, or
human herpesvirus 8, diseases. Clin Microbiol Rev. 2002;15:439–464.
35. Schulz TF. The pleiotropic effects of Kaposi’s sarcoma herpesvirus. J Pathol. 2006;208:187–198.
36. Tomtishen J3. Human cytomegalovirus tegument proteins (pp65, pp71, pp150, oo28). Virol J. 2012;9:22.
37. Alibek K, Kakpenova A, Baiken Y. Role of infectious agents in the carcinogenesis of brain and head and neck cancers.
Infect agent cancer. 2013;8:7.
38. Melnick M, Sedghizadeh PP, Allen CM, Jaskoll T. Human cytomegalovirus and mucoepidermoid carcinoma of sali-
vary glands: cell-specific localization of active viral and oncogenic signalling proteins is confirmatory of a causal
relationship. Exp Mol Pathol. 2012;92:118–125.
39. Saravani S, Kadeh H, Miri-Moghaddam ZekriA, Sanadgol N, Gholami A. Human cytomegalovirus in oral squamous
cell carcinoma in southeast of Iran. Jundishapur J Microbiol. 2015;8:e21838.
40. Steben M, Duarte-Franco E. Human papillomavirus infection: Epidemiologyand pathophysiology. Gynecol Oncol.
2007;107:S2–S5.
41. Bernard HU, Calleja-Macias IE, Dunn ST. Genome variation of humanpapillomavirus types: phylogenetic and medical
implications. Int J Cancer.. 2006;118:1071–1076.
42. Psyrri A, DiMaio D. Human papillomavirus in cervical and head-and-neckcancer. Nat Clin Pract Oncol. 2008;5:24–31.
43. Marklund L, Hammarstedt L. Impact of HPV in oropharyngeal cancer. J Oncol. 2011. doi:10.1155/2011/509036.
44. Dahlen G. Bacterial infections of the oral Mucosa. Periodontology 2000. 2009;49:13–38.
45. Styblok. Overview and Epidemiologic assessment of the current global Tuberculosis situation with an emphasis on
control in developing countries. Review of infectious disease. 1989(11):5338–5346.
46. Kapoor S, Gandhi S, Gandhi N, Singh I. Oral manifestations of tuberculosis. Chrismed J Health Res. 2014;1:11–14.
47. Eng HL, Lu SY, Yang CH, Chen WJ. Oral tuberculosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
1996;81:415–420.
48. Mignogna MD, Muzio LL, Favia G, Ruoppo E, Sammartino G, Zarrelli C. Oral tuberculosis: A clinical evaluation of 42
cases. Oral Dis. 20 0 0;6:25–30.
49. Sierra C, Fortún J, Barros C, Melcon E, Condes E, Cobo J, et al. Extra-laryngeal head and neck tuberculosis. Clin
Microbiol Infect. 20 0 0;6:644–648.
50. Thilander H, Wennestrom A. Tuberculosis of mouth and the surrounding tissues. Oral Surg Oral Med Oral Pathol.
1956;9:858–870.
51. Memon GA, Khushk IA. Primary tuberculosis of tongue. J Coll Physicians Surg Park. 2003;13(I10):604–605.
52. Prabhu SR, Daftary DK, Dholakia HM. Tuberculous ulcer of the tongue: Report of a case. J Oral Surg.
1978;36:384–386.
53. Kumar MP, Kumar MS, Sarkar S, Ramasubramanian S, Anu KJ, Aravindh L. Oral manifestations in patients with
pulmonary tuberculosis. Int J Biol Med Res. 2012;3(2):1565–1567.
54. Bahar S, Zeytinoglu M, Tuncay U, Unal T. Oral mucosal ulceration- a manifestation of previously undiagnosed pul-
monary tuberculosis. JADA. 2004;135:336–340.
55. Turbiner S, Giunta J, Maloney PL. Orofacial tuberculosis of the lip. J Oral Surg. 1975;33:343–347.
56. Reichart P. Facial and oral manifestations in leprosy. An evaluation of seventy cases.. Oral Surg Oral Med Oral Path.
1976;41:385–389.
57. Bucci Jr F, Mesa M, Schwartz RA, McNeil G, Lambert C. Oral lesions in lepromatous leprosy. J Oral Med. 1987;42:
4–6.
58. Pallagatti S, Sheikh S, Kaur A, Aggarwal A, Singh R. Oral cavity and leprosy. Indian Dermatol Online J.
2012;3:101–104.
59. Pellegrino D, Opromolla DV, de Campos I. Leprotic lesions in the oral cavity – their importance in prevention.
Estomatol Cult. 1970;4:123–128.
60. Prabhu SR, Daftary DK. Clinical evaluation of oro-facial lesions of leprosy. Odontostomatol Trop. 1981;4:83–95.
61. Ochandiano S, Acero J, Concejo C, Escrig M, Fernandez J, Garcia-Lechuz JM. Lesiones orales en la lepra lepromatosa.
Presentacion de un caso y r evision de la literatura. Med Oral. 20 0 0;5:316–323.
62. Reichart P, Ananatasan T, Reznik G. Gingiva and periodontium in lepromatous leprosy. Clinical radiological, and
microscopical study. J Periodontol. 1976;47:455–460.
63. MØller-Christensen V, Bakke SN, Melson RS, Waaler E. Changes in the anterior nasal spine of the alveolar process
of the maxillar y bone in leprosy. Int J Lepr. 1952;20:335–340.
64. Scheepers A. Correlation of oral surface temperatures and the lesions of leprosy. Int J Lepr Other Mycobact Dis.
1998;66:214–217.
65. Pinkerton FJ. Leprosy of the ear, nose and throat. Arch Otolaryngol. 1932;16:469–487.
66. Scheepers A, Lemmer J. Erythema nodosum leprosum: a possible cause of oral destruction in leprosy. Int J Lepr.
1992;60:641–643.
67. Smego Jr R, Foglia G. Actinomycosis. Clin Infect Dis. 1998;26:1255–1261.
68. Murray RP, Kobayashi GS, Pfaller MA, Rosental KS. Medical Microbiology. 2nd ed. St Louis, MO: Mosby; 1994.
69. Figueiredo LMG, Trindade SC, Sarmento VA, Oliveira TFL, Muniz WR, Valente ROH. Actinomycotic osteomyelitis of
the mandible: an unusual case. Oral Maxillofac Surg. 2012;17(4):299–302.
70. Sehouli J, Stupin JH, Schlieper U, Kuemmel S, Henrich W, Denkert C, et al. Actinomycotic inflammatory disease and
misdiagnosis of ovarian cancer. A case report. Anticancer Res. 2006;26:1727–1731.
71. Habibi A, Salehinejad J, Saghafi S, Mellati E, Habibi M. Actinomycosis of the tongue. Arch Iranian Med.
2008;11(5):566–568.
72. Jeansonne BG. Periapical actinomycosis: a review. Quintessence Int. 2005;36:149e53.
73. Aldred MJ, Talacko AA. Periapical actinomycosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2003;95:614e20.
ARTICLE IN PRESS
74. Goldstein BH, Sciubba JJ, Laskin DM. Actinomycosis of maxilla: review of literature and report of case. J Oral Surg.
1972;30:362e6.
75. Martin M. The use of oral amoxicillin for the treatment of actinomycosis. Br Dent J. 1984;156:252–254.
76. Martin MV. Antibiotic treatment of cervicofacial actinomycosis for patients allergic to penicillin: a clinical and in
vitro study. Br J Oral Maxillofac Surg. 1985;23::428–434.
77. Ficarra G, Carlos R. Syphilis: the renaissance of an old disease with oral implications. Head Neck Pathol.
2009;3:195e206.
78. Leuci S, Martina S, Adamo D, et al. Oral syphilis: aretrospective analysis of 12 cases and a review of theliterature.
Oral Dis. 2013;19:738–746.
79. Little JW. Syphilis: an update. Oral Surg Oral Med Oral Pathol Oral Radiol Endodontol. 20 05;10 0:3–9.
80. Siqueira CS, Saturno JL, de Sousa SC, da Silveira FR. Diagnostic approaches in unsuspected oral lesions of syphilis.
Int J Oral Maxillofac Surg. 2014 Dec;43(12):1436–1440.
81. Kelner N, Rabelo GD, da Cruz Perez DE, Assunçaõ Jr JN, Witzel AL, Migliari DA, et al. Analysis of nonspecific oral
mucosal and dermal lesions suggestive of syphilis: a report of 6 cases. Oral Surg Oral Med Oral Pathol Oral Radiol.
2014;117(1):1–7.
82. de Pauloab LuizFernandoBarbosa. Joaõ Paulo Silva Servatoa Maiolino Thomaz Fonseca Oliveirab Antonio Francisco
Durighetto Jra Darceny Zanetta-Barbosab Medical Imagery. /. Int J. Infect Dis. 2015;35:40–42.
83. Leão JC, Gueiros LA, Porter SR. Oral manifestations of syphilis. Clinics. 2006;61(2):161–166.
84. Housego T, Wood RE, Grotepass F, Nortje CJ. Repair of a palatal defect associated with late congenital syphilis using
a tongue flap. J Oral Maxillofac Surg. 1998;46:70–73.
85. Ghanem KG, Workowski KA. Management of adult syphilis. Clin Infect Dis. 2011;53(Suppl. 3):S110–S128.
86. Escobar V, Farman AG, Arm RN. Oral Gonococcal Infect. 1984;13(6):549–554.
87. Adams F. Epidemics, Book 3. The Genuine Works of Hippocrates, Francis Adams translations. Baltimore (MD):
Williams and Wilkins; 1939.
88. Adams F. Epidemics, Book 3. The Genuine Works of Hippocrates, Francis Adams translations. Baltimore (MD):
Williams and Wilkins; 1939.
89. Meurman JH, Siikala E, Richardson M, Rautemaa R. Non-Candida albicans Candida yeasts of the oral cavity. In:
Meńdez-Vilas A, ed.. Badajoz (Spain): Formatex; 2007:719–731.
90. Budtz-Jorgensen E. Histopathology, immunology, and serology of oral yeast infections. Diagnosis of oral candidosis.
Acta Odontol Scand. 1990;48(1):37–43.
91. Fotos PG, Vincent SD, Hellstein JW. Oral candidosis. Clinical, historical, and therapeutic features of 100 cases. Oral
Surg Oral Med Oral Pathol. 1992;74(1):41–49.
92. Glick Micheal, Glick Michael. Burket’s Oral Medicine. People’s Medical Publishing House USA; 2014.
93. MacEntee MI, Glick N, Stolar E. Age, gender, dentures and oral mucosal disorders. Oral Dis. 1998;4(1):32–36.
94. Akpan A, Morgan R. Oral candidiasis. Postgrad Med J. 2002;78(922):455–459.
95. Rose JA. Folic-acid deficiency as a cause of angular cheilosis. Lancet. 1971;2(7722):453–454.
96. Redman RS. Prevalence of geographic tongue, fissured tongue, median rhomboid glossitis, and hairy tongue among
3,611 Minnesota school children. Oral Surg Oral Med Oral Pathol. 1970;30:390–395.
97. Neville BradW, et al.. Oral and Maxillofacial Pathology. Elsevier; 2016.
98. Hartwick RW, Batsakis JG. Sinus aspergillosis and allergic fungal sinusitis. Ann Otol Rhinol Laryngol. 1991;100(5 Pt
1):427–430.
99. Page LR, Drummond JF, Daniels HT, Morrow LW, Frazier QZ. Blastomycosis with oral lesions. Oral Surg Oral Med
Oral Pathol. 1979;47(2):157–160.
100. Loh FC, Yeo JF, Tan WC, Kumarasinghe G. Histoplasmosis presenting as hyperplastic gingival lesion. J Oral Pathol
Med. 1989;18(9):533–536.
101. Ru’PON JW. Medical Myeology. Philadelphia: W. B. Saunders; 1982.
102. de Almeida OP, Jorge J, Scully C, Bozzo L. Oral manifestations of paracoccidioidomycosis (South American blastomy-
cosis). Oral Surg Oral Med Oral Pathol. 1991;72(4):430–435.
103. Dodson TB, Perrott DH, Leonard MS. Nonhealing uleeration of oral mucosa. J Oral Maxillofae Surg.
1989;47(8):849–852.
104. Glick M, Cohen SG, Cheney RT, Crooks GW, Greenberg MS. Oral manifestations of disseminated Cryptococ-
cus neoformans in a patient with acquired immunodeficiency syndrome. Oral Surg Oral Med Oral Pathol.
1987;64(4):454–459.
105. Marques SA. Fungal infections of the mucous membrane. Dermatol Ther. 2010;23(3):243–250.
106. Williams DW, Lewis MA. Isolation and identification of Candida from the oral cavity. Oral Dis. 20 0 0;6(1):3–11.
107. O’Shaughnessy EM, Shea YM, Witebsky FG. Laboratory diagnosis of invasive mycoses. Infect Dis Clin North Am.
2003;17(1):135–158.
108. Muzyka BC, Epifanio RN. Update on oral fungal infections. Dent Clin North Am. 2013;57(4):561–581.

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ARTICLE IN PRESS

JID: YMDA [mUS1Ga;October 26, 2018;19:56]

Contents lists available at ScienceDirect

journal homepage: www.elsevier.com/locate/disamonth

Infectious diseases of oral cavityR

Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . .. . ... ... . ... ... . 8

Herpes simplex virus infection

Herpes zoster virus infection

Group 1 Lesions strongly associated with HIV infection

Human papillomavirus-associated oral lesions

Involvement of viral factors with head and neck cancers

Leprosy–non-speciﬁc lesions Enanthem of palate or uvula

Leprosy-speciﬁc lesions Lips Flat-topped nodules

Leprosy is a chronic multi-system infectious disease caused by Mycobacterium leprae.

Actinomycosis is a rare, chronic disease caused by anaerobic Gram-positive bacteria. Humans

Superﬁcial oral fungal infections

Group 1: Candidial lesions conﬁned to oral and perioral areas

Langenbeck in 1839 ﬁrst described a pseudomembranous variant of candidiasis, now com-

Previously referred to as atrophic candidiasis, erythematous candidiasis typically presents

Central papillary atrophy (median rhomboid glossitis)

Deep-seated oral fungal infections

Blastomycosis is a mycotic infection caused by Blastomyces dermatitidis, a dimorphic fungus.

Histoplasomis is an infection caused by H. capsulatum. It usually causes an acute or chronic

Coccidioides immitis is a pathogen that is associated with coccidioidomycosis which is present

Also referred as South American blastomycosis or Lutz’ disease, paracoccidioidomycosis is

Cryptococcosis is a mycostic infection chieﬂy involving lungs that is caused by Cryptococcus

Mucormycosis is an acute opportunistic infection caused by a saprophytic fungus. It is re-

Diagnosis of oral fungal infections

Treatment of oral fungal infections

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