3- Infections of the Oral Mucosa III

7/30/2019 3- Infections of the Oral Mucosa III

1/8

Dr. Tahani Abualteen

1/8

Infections of the oral mucosa III

Fungal Infections Fungal infections of oral mucosa frequently encountered are those due to species of the genus

" Candida" " Candida albicans"is the principle species associated with oral infection,but other species such

as: C. glabrata, C. tropicalis, C. parapsilosis, C. krusei are also pathogenic

Candida species (especially C. albicans) is characterized by the following:o Commensal microorganism in the mouth of about 40% of the population

** Commensalism ) )benefiting from living in the oral cavity without harming

the host or the flora present there

o Dimorphic (exists in two forms; the bud form"present as small oval yeasts in carriers", and

hyphal form "present as elongated rod-like orribbon-like structure in patients)

o Multiply bybudding (production of buds from ovoidyeast cells, buds then separate and grow to form

hyphae)

o Variable carriage rates (carriage rates are increasedin the presence of systemic diseases, pregnancy,

tobacco smokers and denture wearers)

o The primary oral reservoir for the organism in carriers is the posterior dorsum of thetongue (probably due to its rough surface)

o There is overlap in the candidal counts in saliva from carriers and from individuals showinginfection and so isolation of Candida from the mouth of an adult is not confirmatory

evidence of fungal infection and must considered together with clinical findings (presence of a

lesion)

o It is presumed that Candida has a direct etiological relationship with a lesion if hyphae arepresent in smears or in histological sections of the lesion

** The pathogenic form of Candida is the hyphal form that if noticed in the oral cavity it

indicates active fungal infection

** The presence of yeasts alone "bud form" not being regarded as confirmatory evidence

for fungal infection but it might indicate a carrier state** So to diagnose a patient with fungal infection (candidosis) we cant simply rely on the

presence of Candida nor on their count, BUT insteadwe need to see the hyphal form

histologically and the lesion clinically

o Opportunistic pathogen that is waiting for a chance to cause infection whenever the balancebetween the host and the organism is disturbed by different local or systemic factors

Factors predisposing to candidal infection:o They act by altering the homeostatic mechanisms which maintain the host-organism balance,

and the defense mechanisms of the oral cavity in health

Local factors: mucosal trauma, denture (appliance) hygiene, tobacco smoking, carbohydrate-rich diet


2/8


2/8

Xerostomia (either by xerogenic drugs, radiotherapy or Sjgren syndrome) leads todecreased washing effects of saliva and this might enhance the adherence of candida to the

oral mucosa

Age (extremes of age; neonates or elderly people they may not have a competent immunesystem)

Drugs: broad spectrum antibiotics (as they kill bacteria, they disturb the balance betweenbacteria and fungi and this favors candidal growth and proliferation), steroids

(local/systemic cortisol, which cause immune suppression and disturb the balance between

fungi and host), Cytotoxic drugs, immunosuppressive drugs

Systemicdiseases e.g. iron deficiency and megaloblastic anemia, acute leukemia, othermalignancies, diabetes mellitus, AIDS, other immunodeficiency states

Factors protecting against candidal infectiono Non specific factors: shedding of epithelium, salivary flow, Commensal bacteria (oral flora) and

the phagocytic activity of neutrophils and macrophageso Specific factors (targeting the Candida specifically):

Systemic immunity (Serum antibodies) is ofless importance Secretory immunity(secretory antibodies) is more important than systemic immunity in

protection of the oral mucosa

E.g. secretory IgA levels in saliva are raised in patients with oral candidosis and may inhibit

adherence of the Candida to oral epithelium

Cell mediatedimmune responses are impaired in patients with candidal infectionsparticularly in chronic candidosis

Pathogenesis of Candidal infection:o The mechanisms by which Candida species exert a pathological effect on the tissues aren't fully

understood

Adherence (by surface proteins) for colonization, carriage, and the development of infection Secretion of variety of enzymes (such as proteineases) which enable the hyphae to invade

the oral epithelium

Invasion of epithelium by hyphae Secretion of nitrosamine compounds which may play a role in oral carcinogenesis Candidal antigens may induce a delayed hypersensitivity reaction, leading to tissue injury

Classifications of oral and Perioral candidosis:o Group 1: primary oral candidosis (candidosis is confined to oral & Perioral tissues)

Acute: Psuedomembranous Erythematous (atrophic)

Chronic Psuedomembranous Erythematous (atrophic) Hyperplastic (candidal leukoplakia)

Candida associated lesions: Denture stomatitis


3/8


3/8

Angular cheilitis Median Rhomboid glossitis

** In here Candida may be found in association with these mucosal lesions, but a causal

relationship has not been fully established

o Group 2: secondary oral candidosis (oral candidosis is a manifestations of a generalizedsystemic candidosis)

Systemic mucocutaneous candidosis (hereditary and sporadic types associated with systemicdisorders, e.g. endocrine disorders, immunodeficiency states)

Acute Psuedomembranous Candidosis (Thrush) Psuedomembranous candidosis is usually an acute infection but

persistent infection may be seen in immune-compromised

patients, in which case it is described as chronic

Signs and symptoms of acute and chronic types areessentially the same, the duration is the distinguishing feature

Clinically: presents as thick white plaque/coating(psuedomembrane) on affected mucosa, that can be wiped

away/scraped off leaving a red inflamed & often bleeding

base

Psuedomembrane plaque consists ofsuperficial necrotic anddesquamating Keratotic layers of the epithelium infiltrated

by candidal hyphae and yeasts and by an acute inflammatory

exudate

** Psuedomembrane lies on the surface of the tissue and

candidal hyphae are penetrating superficially into the

epithelium to provide anchorage

Lesions arise on any mucosal surface of the mouth Lesions range from small drop-like areas to confluent plaques

over a wide area

Might be associated with pain or burning sensation It is sometimes called disease of diseased, so there should be some predisposing

factors that we need to identify and correct if possible, and this is very important in the

management of this fungal infection

** Predisposing factors: xerostomia, antibiotics, decreased host resistance, 5% of infants, 10% of elderly

Diagnosis:swab (dry scrapping of fungi) orsmear (wet scrapping of fungi) Acute Erythematous (Atrophic) Candidosis:

Erythematous candidosis is usually an acute infection butpersistent infection may be seen in immune-compromised

patients, in which case it is described as chronic

Clinically:presents as red, often painful area of oral mucosacausing generalized pain, discomfort or burning sensation

White plaques and red base


4/8


4/8

It is the only variant of oral candidosis in which pain and discomfort are marked** Epithelium is thin and atrophic and candidal hyphae are penetrating superficially into the

epithelium to provide anchorage

Seen most commonly on the dorsum of the tongue (where thetongue looks red and depapillated) in patients undergoingprolonged corticosteroid or antibiotic therapy (the condition

is sometimes referred to as antibiotic sore tongue)

** Antibiotic therapy alters the oral bacterial flora, and allows

resistant organisms (such as Candida) to flourish and overgrow

** Corticosteroid therapy suppresses the immune system of

the host and allows opportunistic organisms (such as Candida)

to flourish and overgrow

Diagnosis:swab (dry scrapping of fungi) orsmear (wet scrapping of fungi) Chronic Atrophic Candidosis (Candida-associated denture stomatitis):

The most common form of oral candidosis and usually a symptomless condition Regarded as being secondary candidal infection of tissues

modified by continual wearing of ill-fitting dentures

Factors that favor candidal overgrowth and increase theprobability of developing this condition in denture/appliance

wearers:

o Poor denture hygiene (inadequate cleaning of the fittingsurface)

o High-carbohydrate dieto Confined space between the denture and the mucosa

(as in the upper denture)

o Wearing the denture throughout the night Clinically: condition is characterizedby chronic Erythema

and edema of the mucosa directly covered by the denture

(the affected mucosa being clearly delineated by the outline

of the denture)

Palate is almost invariably affected Very uncommon to see lesions related to lower dentures,

probably because they fit much less closely than upper

dentures and so an environment favoring candidal

overgrowth is not present

Condition may also occur under orthodontic appliances Fitting surface of the denture is the reservoir of infection (Candida colonize the denture surface)

because Candida adheres readily to acrylic and microscopic irregularities on the fitting surface

which provide a suitable environment for growth and retention of the organism which will later

on irritate the contacting mucosa causing inflammatory response

** If biopsy is performed, we will NOT see Candidal hyphae invading tissues but rather they arepresent on the fitting surface of the denture, so there is minimal or no candidal invasion of mucosa


5/8


5/8

Clinically, three patterns of inflammation can be identified (Newtons classification):o Pin-pointareas of Erythema (localized inflammation)o Diffuse Erythema (generalized inflammation)most commono Erythema associated with a granular or multinodular mucosal surface(chronic papillary

hyperplasia of the palate)

uncommon Improving the denture hygiene is the key to the management of this condition

Chronic Hyperplastic Candidosis (Candidal Leukoplakia) Clinically: presents as persistent whitepatch on the oral

mucosa thatcant be removed by scraping and which is

indistinguishable from non-homogenous leukoplakia

(speckled/nodular)

- Characteristically, lesions present as white patches ofirregular thickness and density with a rough or

nodular surface

- Areas of Erythematous mucosa are sometimes presentwithin the plaque

Lesions are seen most frequently on the buccal mucosaadjacent to the commissure of the lips

Lesions are roughly triangular in shape with theirbasedirected anteriorly and the apex pointing posteriorely

Lesions are usually bilateral Lesions are often associated with angular cheilitis When multiple sites are affected, the term "chronic

multifocal oral candidosis" is sometimes applied In many patients there is a strong association with tobacco

smoking

** Other local factors, such as: denture wearing and

occlusal friction, may also be involved

Histologically:o Epithelium shows hyperkeratosis and prominent irregular acanthosiso Candidal hyphae invade superficially into the Parakeratin layer, and NEVER penetrate

deeper into the prickle cell layer

o Areas of atrophic epithelium may be present within the lesion and in these areas superficiallayers of Candida-infected Parakeratin may be missing and this is responsible for the speckled

erythematous appearance seen clinically

o Edema & neutrophils infiltration of the Parakeratin withsuperficial microabscess formationo Variable inflammatory infiltrate is present throughout the prickle cell layer and in the lamina

propria

** Whenever inflammatory infiltrate is seen in the superficial layers (even if candidal hyphae

aren't seen), PAS stain is needed to confirm or exclude candidosis

** PAS (periodic acid Schiff) stain is a special dye that stains the carbohydrate-rich wall inCandida with a red or pink color


6/8


6/8

It is NOT clear yet whetherchronic hyperplastic candidosis is primarily leukoplakia with asecondary candidal infection (e.g. Candida is a secondary colonizer), or whether it is primarily a

chronic candidal infection (e.g. Candida is a causative agent) which in time leads to epithelial

dysplasia

o Some argue that Candida is causative because many lesions heal or regress with antifungaltherapy

o Others argue that Candida is a secondary colonizer because Candida tends to adhere and live inrough altered epithelium (e.g. leukoplakia)

Diagnosis: biopsy (to confirm presence of hyphae and detect presence/degree of dysplasia) Prognosis:

o Premalignant lesiono 50% of cases are associated with epithelial dysplasia

** In some cases this dysplasia resolves following treatment. In such cases the dysplasia can be

described as "reactive dysplasia" in response to irritation from candidal products and the

associated chronic inflammation

** About 15% of cases progress to"true dysplasia"

** As with idiopathic leukoplakia, the severity of the dysplasia is increased in speckled, non-

homogeneous lesions

** Most of candidal Leukoplakias are non homogenous increasing the riskfor dysplasia or

malignant transformation

** Candida can generate carcinogens like nitrosamine increasing the riskfor dysplasia or

malignant transformation

Candida-associated angular Cheilitis: Angular (occurs at the corners of the mouth) chelitis

(inflammation of the lips)

It is a multifactorial disease of infectious origin


7/8


7/8

The condition occurs predominantly in denture wearers and is seen in about 30% of patients withdenture stomatitis and less frequently with other types of oral candidosis (e.g. chronic

hyperplastic candidosis)

The condition can be due to fungal infection (e.g. Candida)orbacterial infection (e.g. staphylococcus aureus or lessfrequently streptococci) orcombined infection

Clinically: characterized by Erythema, soreness, cracks,fissures, crusts and pain at the corners of the mouth

(commissure area)

There are many contributory factors that may play a rolein the pathogenesis of the condition:

o Incorrectly designed or old denture with loss ofvertical dimension(MAIN factor) result in deep

folds of skin at angles of mouth folds predispose to

infection in the skin as a result ofcontinual wetting by

saliva leading to cracks, fissures, crusts, and pain in

commissure area

o Nutritional deficiencies (like iron, B12, or folic aciddeficiency)

Candida-associated median Rhomboid Glossitis: Median (occurs in the midline), Rhomboid (due to its shape), glossitis (inflammation of the tongue) Occurs in the midline of the dorsal surface of the tongue,

just anterior to the foramen cecum (where the tonguelooks red and depapillated)

Clinically: lesion is roughly rhomboidal in shape. Thesurface appears reddish in color and may be smooth,

nodular, or fissured

Usually asymptomatic The pathogenesis of the lesion is uncertain (etiological

debate!)

** Some argue that the lesion is a developmental lesion

arising at the junction between the anterior and the posteriorparts of the tongue (they thought that this area may not

develop well) and this suggestion cant be definitely

excluded

** Others argue that the lesion is a localized form ofchronic fungal infection as in most of the cases;

lesions are associated with candidal infection (although it is unlikely that the area will re-papillate

following antifungal therapy)

Opposing kissing lesion may be seen on the palate (due to the contact between tongue & palate) andthe term "chronic multifocal oral candidosis" has been used to describe this

** Palatal lesion is not necessarily red; it might be whitepsuedomembranous** Opposing "kissing" lesion on the palate can be also seen in acute erythematous candidosis

D/D: Erythematous candidosis, however

patients history and the location of the

lesion guide the correct diagnosis


8/8


8/8

Chronic mucocutaneous candidosis (CMC): Rare group of disorders characterized by persistent superficial

candidal infections of mucosae, nails and skin

Oral mucosa is involved in almost all cases Oral lesions resemble those seen in chronic hyperplasticcandidosis and may involve any part of the mucosa Oral lesions might be multifocal CMC may be inherited or acquired, and may be associated with

endocrine disorders, or immunodeficiency

Oral manifestations of the systemic/deep visceral mycoses: Rare outside endemic areas (found mainly in south America and parts

of USA)

Oral lesions are uncommon, but may present as non-specific ulceration or as nodular granulomatousareas

Lesions are NOT caused by Candida (Candida cause superficial lesions only) Examples ofdeep visceral mycoses which may be associated with oral lesions are:

o Blastomycosiso Histoplasmosiso Zycomycosiso Coccidiodomycosis

Clinical aspects:

- Psuedomembranous candidosis (thrush) & chronic hyperplastic candidosis present as whitepatches, differences between the two include:

1. Psuedomembrane can be wiped offBUT white patch of hyperplastic type is fixed2. Psuedomembranous occur anywhere in the mouth BUT hyperplastic type typically involves

the commissures

- Erythematous candidosis & denture stomatitis present as red patches, differences between the twoinclude:

1. Erythematous involves mainly tongue BUT denture stomatitis confined to palate2. Erythematous usually sore BUT denture stomatitis usually symptomless

- Angular chelitis may be associated with denture stomatitis or chronic hyperplastic candidosis- Median rhomboid glossitis present as reddish smooth/nodular area anterior to foramen cecumPathological aspects:

- Hyphae invade the superficial Parakeratin layer except in denture stomatitis- No hyphal invasion of epithelium in denture stomatitis, organism only colonizes denture base- Prominent acanthosis in chronic hyperplastic candidosis- Dysplasia in chronic hyperplastic candidosis

Diagnosis of fungal infection:

o Patients historyo Clinical featureso Swab and stained smearo Swab and cultureo Biopsy with PAS

3- Infections of the Oral Mucosa III

Documents

Transcript of 3- Infections of the Oral Mucosa III