Infections of the Oral Mucosa 2

Dr. Rima Safadi

Fungal Infections
Candida albicans

Dimorphic Multiply by budding Commensal Others like C. are also pathogenic

glabrata, tropicalis, parapsilosis, C. krusei

Fungal Infections
Candida albicans

Variable carriage rates around 40%... Mainly on the tongue Candidal counts overlap between patients (infection) and carriers Presence of hyphae in smears is important for diagnosis

Candidosis

Opportunistic pathogen Disturbance of balance between host and organism (homeostatic balance) Factors: local and systemic

Candidosis

Factors predisposing to candidal infection

Local factors: trauma, denture hygiene, tobacco smoking, carbohydrate-rich diet Age Drugs: broad spectrum AB, steroids, cytotoxic drugs Xerostomia Systemic diseases

Candidosis

Protection against candidal infection

Non specific factors: shedding of epithelium, salivary flow, commensal bacteria Specific:

Serum

antibodies: less important Secretory immunity is more important (it decreases adherence of candida) Cell mediated

Candidosis

Pathogenesis of Candidal infection

Adherence Secretion of enzymes: proteineases Invasion of epithelium by hyphae Secretion of nitrosamine compounds ? Type 4 hypersensitivity to candidal pathogens

PAS stain

Classification of Oral Candidosis

Classifications: acute or chronic, oral or extraoral

Acute: Psuedomembranous Erythematous (atrophic) Chronic Psuedomembranous Erythematous (atrophic)

Hyperplastic (candidal leukoplakia)

Classification of Oral Candidosis

Candida

associated lesions:

Denture

stomatitis Angular cheilitis Median Rhomboid glossitis

Secondary
Systemic

oral candidosis:

mucocutanous candidosis

Pain or burning Predisposing:

Acute Pseudomembranous Candidosis (Thrush)

xerostomia, antibiotics decreased host resistance 5 % of infants, 10% of elderly

White

plaques and red base

Acute Pseudomembranous Candidosis (Thrush)

Acute Erythematous (Atrophic) Candidosis

(antibiotic sore tongue) Generalized pain, burning, erythema Prolonged corticosteroids or antibiotics Red and painful

Chronic Atrophic Candidosis (Candidaassociated denture stomatitis)

Secondary infection by Candida in tissues modified by continual wearing of dentures Poor denture hygiene High carbohydrate diet May be asymptomatic Candida colonize the denture surface Minimal or no candidal invasion of mucosa

1.

2.
3.

3 patterns of inflammation (Newtons classification): Pinpointed erythema Diffuse erythema Granular or multinodular (chronic inflammatory papillary hyperplasia)

Chronic Hyperplastic Candidosis (Candidal Leukoplakia)

Persistent white patch Speckled/nodular Most frequent location: buccal mucosa at commissures Triangular Bilateral Associated with angular cheilities? Strong association with smoking

Local factors?

Chronic Hyperplastic Candidosis (Candidal Leukoplakia)

Can be multifocal

Chronic multifocal oral candidosis

Chronic Hyperplastic Candidosis (Candidal Leukoplakia)

Chronic Hyperplastic Candidosis (Candidal Leukoplakia)

PAS Stain

Chronic Hyperplastic Candidosis (Candidal Leukoplakia)

Premalignant?????
50% associated with epithelial dysplasia 15% progress to true dysplasia

Most of candidal leukoplakias are non homogenous

Candida can generate carcinogenes like nitrosamine

Chronic Hyperplastic Candidosis (Candidal Leukoplakia)

Premalignant??????

Is candida a secondary infection of a pre existing leukoplakia?

Some lesions respond to antifungal therapyetiologic role

Angular Cheilitis

Fungal or bacterial or combined

Angular Cheilitis

Multifactorial disease of infectious origin

Candida or Staph aureus or Streptoccocci

Mainly in denture wearers

30% of patient with denture stomatitis have anguar cheilitis

Angular Cheilitis

Cracks, fissures, crusts, pain in commissure area Loss of vertical dimension Deep folds of skin at angles of mouth

Continual wetting by saliva

Nutritional deficiencies

PAS stain modified for fungi

Median Rhomboid Glossitis

Just anterior to foramen cecum Red depapillated smooth or fissured asymptomatic Etiologic debate

Developmental or chronic candidal infection

Opposing lesion on the palate may be seen

Multifocal candidosis

Chronic mucocutanous candidosis

Persistent superficial infection of: skin, mucosa, nails Oral mucosa involved in most cases Orally: similar to candidal leukoplakia May be multifocal

Deep fungal infections

Non specific ulceration Or Granulomatous areas

Blastomycosis

Histoplasmosis

Zycomycosis

HIV infection and AIDS

Sero-conversion: detection of HIV antibodies in blood

Sero-postitive for many years later on Persistent generalized lymphadenopathy AIDS related complex: persisitent pyrexia, lymphadenopathy, diarrhea, weight loss, fatigue and malaise Final Stage: Fully developed AIDS: opportunistic infections, Kaposi sarcoma, non Hodgekins lymphoma.

in 3 months May have also acute symptoms

Infection by the virus means: virus binds to: CD4 T lymphocytes, macrophages, CNS cells, endothelial cells CD4 cells die leading to decrease number of T helper Impaired immunity particularly against: viruses, fungi and encapsulated bacteria.

Table 11.5 in your text book groups the lesions associated with AIDS

Oral Manifestations of HIV infection

Oral candidosis Most frequent oral manifestation Azole resistant species Psuedomembranous and erythematous are most frequent types. Chronic, multifocal May involve any part of the oral mucosa

Prevalence:

Hyperplastic type involves buccal mucosa rarely commissures

20% of HIV seropositve positive patients 70% of AIDS have oral candidosis Prev. decreasing with introductions of HAART

Viral Infections

HSV, HZV: more severe and extensive than HIV negative pts Dissimenated CMV infection Kaposi sarcoma and HHV8 EBV and Hairy leukoplakia Oral Warts is increasing.

Hairy Leukoplakia

Common in late stage HIV infection indicating AIDS Vertical white folds on lateral border of the tongue, bilaterally White patch that can not be removed May have smooth flat surface May have candidal hyphae but as secondary

Hairy Leukoplakia

Opportunistic infection of oral epithelium by EBV

After primary infection shedding from oropharynx or salivary glands persists Minor trauma to tongue facilitates infection with virus Marked reduction of langerhans cells

Hairy leukoplakia

In 20-25% of patients May indicate the development of AIDS Can occur in pts receiving immunosuppressive medications NOT pre malignant

Hairy leukoplakia

Acanthosis Parakeratosis Finger like surface projections of parakeratin Absence of inflammatory cells in epithelium and lamina propria Swollen or balloon cells with prominent cell boundaries in pricke cell layer below parakeratin Perinuclear vaculization, small drak nuclei: koilocyte-like cells

HIV associated periodontal diseases

1. Linear gingival erythema 2. NUG 3. NUP

HIV-Gingivitis linear gingival erythema

Linear band of erythema free gingival margin

Not responsive to plaque control

Gingival hyperaemia due to release of vasoactive cytokines rather than inflammation Has been associated with C.

albicans

<10% of AIDS patietns

Necrotizing Ulcerative Periodontitis

Severe rapidly destructive process Necrosis of gingival and periodontal tissues Exposure of alveolar bone and sequestration Due to sever impairment of local defensive mechanisms like reduction in CD4 cells Defects usually localized Not responsive to conventional periodontal therapy

ANU periodontitis

Acute Necrotizing Ulcerative Gingivitis

Kaposis sarcoma
Clinical features Commonest tumor associated with AIDS
But with low prevalence especially with medications

Male more than females Associated with HHV8 Multifocal tumor: skin and mucosa Mainly palatal lesion, tip of the nose

Kaposis Sarcoma

Kaposis sarcoma

Clinical:

Kaposis sarcoma can be a surface lesion or a soft tissue enlargement. red purple patch macular Plaque Nodular Multiple lesions common

Kaposi sarcoma

Proliferating endothelial cells Cleft like vascular channels Extravasated RBC Inflammation Occasional atypical cells

Later stages more atypical cells Early stages difficult to differentiate it from other vascular lesions

Slit-like vessels

Oral manifestations of HIV infection

Non Hodgkins lymphoma Neurological disturbances:

HIV is neurotropic may directly involve CNS Facial nerve palsy

Atypical ulceration: resemble aphthous stomatitis may be associated with CMV Salivary gland disease:

xerostomia Salivary gland enlargement associated with lymphocytic infiltrate Lymphoepithelial cysts

HIV associated HSV infection

HIV associated HZV infection

HIV thrombocytopenic purpura, autoimmune response

HIV oral ulceration

HIV lymphoma

????