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associated with types 6 and 11. Currently, a vaccine targeting multiple high- risk and low- risk types
6 and 11 is available and effective if given before exposure(54– 60).
19.2.8.2 Papilloma
19.2.8.2.1 Clinical Features
Papilloma is the most common presentation of HPV infection(57). These benign lesions can occur
at any age and at any oral mucosal site. Papillomata are usually single, white lesions with finger- like
processes most often occurring on the palate and tongue (Figures19.16 and19.17).
19.2.8.2.2 Management
Surgical removal is the treatment of choice.
19.2.8.2.3 Condyloma Acuminata
Condyloma (condyloma acuminatum) is a manifestation of HPV infection. Skin- coloured, fleshy
papules in the anogenital region characterise the condition. Rarely, oral mucosa may present
condyloma acuminata(61).
Figure19.16 Papilloma in the right
hard palate.
Figure19.17 Papilloma in the lateral tongue.
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19.2.8.2.4 Clinical Features
Condylomas are most often associated with HPV types 6 and 11. Clinically, these lesions are similar
in appearance to papillomas but are usually more extensive andmore clustered. Also, condylomas
are known to be more diffuse and deeply rooted than papillomas. These lesions are commonly
found on the labial mucosa, soft palate and lingual frenum. Condylomas can occur anywhere in
the oral cavity and are usually multiple, asymptomatic, pink, exophytic masses larger than
papillomas (Figure19.18). These occur more frequently inimmunocompromised patients. Most
often, condylomas in the oral cavity are related to oral– genital contact.
19.2.8.2.5 Management
Conservative surgical excision is the treatment of choice. Cryotherapy, systemic or intralesional
interferon, and topical cidofovir can be effective.
19.2.9 HIV/AIDS
19.2.9.1 Pathogenesis
HIV 1 and 2 are retroviruses in the Retroviridae family. It is thought that human infection occurred
in the early 1900s by transmission of a simian immunodeficiency virus acquired during the killing/
eating of bushmeat. It was only when the immune deficiency- related illnesses of Kaposi’s sarcoma
and Pneumocystis jirovecii pneumonia became evident in Western European and American men in
the early 1980s that the world’s attention was drawn to the problem.
Most infections outside of Africa are HIV- 1. HIV- 2 causes a similar immunodeficiency state,
although the disease course is more slowly progressive and less aggressive as a rule. The routes
ofinfection include contaminated IV or IM needles, mucosal contamination by infected semen or
vaginal fluid and, previously, infected blood/blood products.
HIV infection results in a devastating collapse of the immune system, rendering the individual
prone to opportunistic infections, especially fungal and viral. Oral viral (HSV and Varicella Zoster)
and fungal infections (oral candidiasis) are common in HIV infections.
Non- Hodgkin and Hodgkin’s lymphomas have significantly increased due to many factors,
including activation of the oncogenic viruses Epstein- Barr virus (EBV) and Kaposi’s sarcoma associated herpesvirus (KSHV). Epithelial cancers such as anal and cervical carcinoma are increased
as well due to activation of HPV.
331
Figure19.18 Condyloma in the
floor of the mouth in an
immunocompromised adult.
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332
The immunologic hallmark of HIV infection is the profound reduction in CD- 4+ lymphocytes,
reversing the normal CD4/CD8 ratio and causing multifactorial, adaptive immune system
dysregulation. HIV does, however, negatively affect the innate immune response as well. The
virus initially is carried to regional lymph nodes by dendritic antigen- presenting cells in those
infections acquired through mucosal or skin contact followed by infection of the CD4 T- cells
within the nodes. If infection occurs through IV drug use or infected blood products (virtually
eliminated in countries with developed medical systems), CD4 cells are infected directly in the
bloodstream. Widespread viral replication occurs throughout the lymphoid system, particularly
in the gut- associated lymphoid tissue (GALT). Although anti- HIV antibodies are produced,
they are insufficiently neutralising to control viral replication. The quantitative determination
of CD4 cells in the peripheral blood and the HIV viral load are the best current markers of disease control and infectivity.
The gradual depletion of CD4 cells is complex. Still, it involves initiation of apoptosis in infected
cells, destruction of infected CD4 cells by CD8 cells and initiation of cell death in uninfected CD4
cells through pyroptosis(62– 65).
Modes of transmission include sexual contact, IV drug use, transfusion of blood or blood products (previously) and perinatal transmission. AIDS infection is characterised by CD4levels lower
3
than 200/mm
. Various oral lesions include linear gingival erythema, NUG and NUP. Candidiasis,
hairy leukoplakia, Kaposi sarcoma and condylomas occur as well.
19.2.10 Oral andMaxillofacial Fungal Infections
Candida albicans is the most common fungal commensal in the oral cavity. Candida becomes
active following prolonged antibiotic therapy, systemic corticosteroids/steroid inhalers, dry
mouth, 24/7 denture wearing, smoking and immunocompromised status. Acute candidiasis is
commonly called thrush or pseudomembranous candidiasis. Chronic candidiasis presents as
erythematous candidiasis, denture stomatitis and angular cheilitis. Median rhomboid glossitis, now known as central papillary atrophy, offers midline erythematous areas on the dorsal
tongue(66, 67).
19.2.10.1 Pathogenesis ofCandidiasis
Commensal microorganisms such as Candida sp. reside on the surface of the mucosa without
affecting human health. Candida, however, becomes pathologic when environmental changes
occur causing superficial and invasive infections. Antibiotics, steroids, chemotherapeutics, xerostomia and nutritional deficiency alter the attachment of Candida to the mucosal surface, thus
causing candidiasis. In xerostomic patients, there is a decrease in the salivary antifungal agents
such as lactoferrin, lysozyme, histatins and immunoglobulins, allowing the proliferation of
Candida. Reduction in mucosal integrity due to nutritional deficiency also contributes to
infection(66, 67).
In its yeast form, Candida reversibly attaches to the oral epithelial cells through electrostatic
interactions. Cell- wall receptors mediate the attachment via the family of glycoproteins. The yeast
changes morphology to a filamentous hyphal form whenever the host defence mechanism
isimpaired, known as phenotypic switching– critical for the host tissue invasion. Extracellular
hydrolytic enzymes produced by Candida mediate the destruction of host tissue and subsequent
invasion. Candida can form biofilms on denture bases, increasing virulence and fungal
susceptibility(66, 67).
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19.2.10.2 Clinical Features
Patients present with burning mouth and/or altered taste of a few days duration with generalised,
wipeable, white plaques with the appearance of ‘cottage cheese’. On wiping these white plaques,
erythema with spotty bleeding is characteristic (Figure19.19). Erythematous candidiasis or denture stomatitis occurs mainly on the palate with a history of denture- wearing 24/7 or an ill- fitting
denture (Figure19.20). This is usually chronic and asymptomatic. Angular cheilitis appears as a
fissured lesion on an erythematous base at the angle of the mouth (Figure19.21). Central papillary
atrophy presents as rhomboid redness or white areas in the mid- dorsal tongue (Figure 19.22).
Typically, similar lesions are seen on the palate. The diagnosis is usually established clinically.
Asmear of the area, examined microscopically, will assist in diagnosis(66, 67).
19.2.10.3 Management
Clotrimazole troches, nystatin suspension or cream, are used to manage oral candidiasis. If patients
are dentulous, avoid using nystatin as they contain sugar. Clotrimazole troches will help in controlling oral infections. Managing oral candidiasis in denture patients requires nystatin cream or powder applied to the denture or a suspension as a rinse. Disinfection of dentures is done by soaking
the dentures overnight in 1:10 dilute household bleach. Angular cheilitis are managed by applying
an equal amount of clotrimazole and 1% hydrocortisone cream to the angle of the lip. In managing
candidiasis, the previously mentioned predisposing factors should be addressed.
Figure19.19 Pseudomembranous
candidiasis presenting as wipeable
white plaques.
333
Figure19.20 Erythematous
candidiasis in a denture wearer.
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334
Figure19.21 Angular cheilitis showing as
an erythematous area at the commissure.
Figure19.22 Central papillary
atrophy is noted as the erythematous
area on the dorsal tongue.
19.2.11 Deep Fungal Infections
The environmental dimorphic fungus, Histoplasma capsulatum causes histoplasmosis. This
organism thrives in moist, nitrogen- rich soil enriched by bat and chicken faeces. Bats may harbour
Histoplasma in their gut, but birds are not infected. Human infection results when the microconidia are inhaled in dried soil or dust. Bat caves, bat guano and chicken coups have been associated
with infectious outbreaks.
Most human infections are asymptomatic due to the small inoculum and the ability of the immune
system to isolate organisms by forming granulomas. Immune- compromised individuals may develop
severe pneumonia or disseminated infection, usually through reactivation of latent pulmonary infection. Following inhalation of the microconidia, the fungus converts to the yeast form and is ingested
by pulmonary macrophages, where it multiplies. Histoplasma resists degradation within the phagocytic lysosome by inhibiting the production of activated nitrogen and oxygen species and lysosomal
t.me/Dr_Mouayyad_AlbtousH
References
proteases. The organism activates apoptosis, thereby spreading to other macrophages which then may
disseminate to regional lymph nodes and elsewhere, especially in the setting of immunosuppression
(AIDS, corticosteroid therapy, chemotherapy). The oral cavity is not primarily infected by histoplasmosis. Oral lesions are considered a manifestation of disseminated disease(68).
Oral deep fungal infections such as histoplasmosis occur in the elderly and immunocompromised
patients. These infections primarily infect the lungs and are rare in the oral cavity. The lesions
may appear anywhere in the oral cavity and present as single chronic, painful or painless ulcerations resembling oral squamous cell carcinomas. A biopsy is required for diagnostic confirmation. Amphotericin B or itraconazole have been used in treatment along with debridement of
the ulcer.
19.3 Summary
Knowledge of the pathogenesis of tissue injury caused by various microbial organisms and the
mechanisms of tissue damage is essential for those treating oral infections. The complexity of tissue injury and the inflammatory/immune response induced by bacterial, fungal and viral organisms of oral infections are discussed. The aetiology, clinical features and management of most
common microbial diseases are briefly reviewed with emphasis on pathogenesis.
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