Template:Short description Template:Infobox medical condition (new) Oral candidiasis (Acute pseudomembranous candidiasis), also known among other names as oral thrush,<ref name="Andrews"/> is candidiasis that occurs in the mouth. That is, oral candidiasis is a mycosis (yeast/fungal infection) of Candida species on the mucous membranes of the mouth.

Candida albicans is the most commonly implicated organism in this condition. C. albicans is carried in the mouths of about 50% of the world's population as a normal component of the oral microbiota.<ref name="Kerawala 2010">Template:Cite book</ref> This candidal carriage state is not considered a disease, but when Candida species become pathogenic and invade host tissues, oral candidiasis can occur. This change usually constitutes an opportunistic infection by normally harmless micro-organisms because of local (i.e., mucosal) or systemic factors altering host immunity. Template:TOC limit

ClassificationEdit

Traditional classification of oral candidiasis.<ref name="OMF medicine textbook" />
  • Acute candidiasis:
    • pseudomembranous candidiasis (oral thrush)
    • atrophic candidiasis
  • Chronic candidiasis:
    • atrophic candidiasis
    • hyperplastic candidiasis
      • chronic oral candidiasis (Candida leukoplakia)
      • candidiasis endocrinopathy syndrome
      • chronic localized mucocutaneous candidiasis
      • chronic diffuse candidiasis.

Classification of oral candidiasis.<ref name="OMF medicine textbook" />
  • Primary oral candidiasis (group I)
    • Pseudomembranous (acute or chronic)
    • Erythematous (acute or chronic)
    • Hyperplastic: plaque-like, nodular
    • Candida-associated lesions: Denture related stomatitis, angular stomatitis, median rhomboid glossitis, linear gingival erythema
  • Secondary oral candidiasis (group II)
    • Oral manifestations of systemic mucocutaneous candidiasis (due to diseases such as thymic aplasia and candidiasis endocrinopathy syndrome)

Oral candidiasis is a mycosis (fungal infection). Traditionally, oral candidiasis is classified using the Lehner system, originally described in the 1960s, into acute and chronic forms (see table). Some of the subtypes almost always occur as acute (e.g., acute pseudomembranous candidiasis), and others chronic. However, these typical presentations do not always hold true, which created problems with this system. A more recently proposed classification of oral candidiasis distinguishes primary oral candidiasis, where the condition is confined to the mouth and perioral tissues, and secondary oral candidiasis, where there is involvement of other parts of the body in addition to the mouth. The global human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) pandemic has been an important factor in the move away from the traditional classification since it has led to the formation of a new group of patients who present with atypical forms of oral candidiasis.<ref name="OMF medicine textbook" />

By appearanceEdit

Three main clinical appearances of candidiasis are generally recognized: pseudomembranous, erythematous (atrophic) and hyperplastic.<ref name="Samaranayake 2009" /> Most often, affected individuals display one clear type or another, but sometimes there can be more than one clinical variant in the same person.<ref name="OMF path textbook" /> Template:Multiple image

PseudomembranousEdit

Acute pseudomembranous candidiasis is a classic form of oral candidiasis,<ref name="Greenberg 2008" /> commonly referred to as thrush.<ref name="Samaranayake 2009" /> Overall, this is the most common type of oral candidiasis,<ref name="Bruch 2010" /> accounting for about 35% of oral candidiasis cases.<ref name="Rhodus 2012" />

It is characterized by a coating or individual patches of pseudomembranous white slough that can be easily wiped away to reveal erythematous (reddened), and sometimes minimally bleeding, mucosa beneath.<ref name="Bruch 2010" /> These areas of pseudomembrane are sometimes described as "curdled milk",<ref name="Samaranayake 2009" /> or "cottage cheese".<ref name="Bruch 2010" /> The white material is made up of debris, fibrin, and desquamated epithelium that has been invaded by yeast cells and hyphae that invade to the depth of the stratum spinosum.<ref name="Samaranayake 2009" /> As an erythematous surface is revealed beneath the pseudomembranes, some consider pseudomembranous candidiasis and erythematous candidiasis stages of the same entity.<ref name="Samaranayake 2009" /> Some sources state that if there is bleeding when the pseudomembrane is removed, then the mucosa has likely been affected by an underlying process such as lichen planus or chemotherapy.<ref name="OMF path textbook" /> Pseudomembraneous candidiasis can involve any part of the mouth, but usually it appears on the tongue, buccal mucosae or palate.<ref name="Bruch 2010" />

It is classically an acute condition, appearing in infants, people taking antibiotics or immunosuppressant medications, or immunocompromising diseases.<ref name="Greenberg 2008" /> However, sometimes it can be chronic and intermittent, even lasting for many years. Chronicity of this subtype generally occurs in immunocompromised states, (e.g., leukemia, HIV) or in persons who use corticosteroids topically or by aerosol.<ref name="Samaranayake 2009" /> Acute and chronic pseudomembranous candidiasis are indistinguishable in appearance.<ref name="Greenberg 2008" />

ErythematousEdit

Erythematous (atrophic) candidiasis is when the condition appears as a red, raw-looking lesion.<ref name="Rhodus 2012" /> Some sources consider denture-related stomatitis, angular stomatitis, median rhomboid glossitis, and antibiotic-induced stomatitis as subtypes of erythematous candidiasis, since these lesions are commonly erythematous/atrophic. It may precede the formation of a pseudomembrane, be left when the membrane is removed, or arise without prior pseudomembranes.<ref name="Greenberg 2008" /> Some sources state that erythematous candidiasis accounts for 60% of oral candidiasis cases.<ref name="Rhodus 2012">Template:Cite journal</ref> Where it is associated with inhalation steroids (often used for treatment of asthma), erythematous candidiasis commonly appears on the palate or the dorsum of the tongue.<ref name="Greenberg 2008" /> On the tongue, there is loss of the lingual papillae (depapillation), leaving a smooth area.<ref name="OMF path textbook" />

Acute erythematous candidiasis usually occurs on the dorsum of the tongue in persons taking long term corticosteroids or antibiotics, but occasionally it can occur after only a few days of using a topical antibiotic.<ref name="Soames 1999" /> This is usually termed "antibiotic sore mouth", "antibiotic sore tongue",<ref name="Soames 1999" /> or "antibiotic-induced stomatitis" because it is commonly painful as well as red.

Chronic erythematous candidiasis is more usually associated with denture wearing (see denture-related stomatitis).Template:Cn

HyperplasticEdit

This variant is also sometimes termed "plaque-like candidiasis" or "nodular candidiasis".<ref name="Greenberg 2008" /> The most common appearance of hyperplastic candidiasis is a persistent white plaque that does not rub off. The lesion may be rough or nodular in texture.<ref name="Coulthard 2008" /> Hyperplastic candidiasis is uncommon, accounting for about 5% of oral candidiasis cases,<ref name="Rhodus 2012" /> and is usually chronic and found in adults. The most common site of involvement is the commissural region of the buccal mucosa, usually on both sides of the mouth.<ref name="Coulthard 2008" />

Another term for hyperplastic candidiasis is "candidal leukoplakia". This term is a largely historical synonym for this subtype of candidiasis, rather than a true leukoplakia.<ref name="pmid12907694">Template:Cite journal</ref> Indeed, it can be clinically indistinguishable from true leukoplakia, but tissue biopsy shows candidal hyphae invading the epithelium. Some sources use this term to describe leukoplakia lesions that become colonized secondarily by Candida species, thereby distinguishing it from hyperplastic candidiasis.<ref name="Coulthard 2008">Template:Cite book</ref> It is known that Candida resides more readily in mucosa that is altered, such as may occur with dysplasia and hyperkeratosis in an area of leukoplakia.Template:Cn

Associated lesionsEdit

Candida-associated lesions are primary oral candidiases (confined to the mouth), where the causes are thought to be multiple.<ref name="Samaranayake 2009" /> For example, bacteria as well as Candida species may be involved in these lesions.<ref name="Greenberg 2008" /> Frequently, antifungal therapy alone does not permanently resolve these lesions, but rather the underlying predisposing factors must be addressed, in addition to treating the candidiasis.<ref name="Samaranayake 2009" />

Angular cheilitisEdit

File:Angular cheilitis1.jpg
Angular cheilitis

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} Angular cheilitis is inflammation at the corners (angles) of the mouth, very commonly involving Candida species, when sometimes the terms "Candida-associated angular cheilitis",<ref name="Soames 1999" /> or less commonly "monilial perlèche" are used.<ref name="Park 2011">Template:Cite journal</ref> Candida organisms alone are responsible for about 20% of cases,<ref name="OMF path textbook" /> and a mixed infection of C. albicans and Staphylococcus aureus for about 60% of cases.<ref name="Kerawala 2010" /> Signs and symptoms include soreness, erythema (redness), and fissuring of one, or more commonly both the angles of the mouth, with edema (swelling) seen intraorally on the commissures (inside the corners of the mouth). Angular cheilitis generally occurs in elderly people and is associated with denture related stomatitis.<ref name="Scully 2013" />

Denture-related stomatitisEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} This term refers to a mild inflammation and erythema of the mucosa beneath a denture, usually an upper denture in elderly edentulous individuals (with no natural teeth remaining). Some report that up to 65% of denture wearers have this condition to some degree.<ref name="Salerno 2011" /> About 90% of cases are associated with Candida species,<ref name="Scully 2013" /> where sometimes the terms "Candida-associated denture stomatitis",<ref name="Salerno 2011">Template:Cite journal</ref> or "Candida-associated denture-induced stomatitis" (CADIS),<ref name="Tyldesley 2003" /> are used. Some sources state that this is by far the most common form of oral candidiasis.<ref name="Tyldesley 2003">Template:Cite book</ref> Although this condition is also known as "denture sore mouth",<ref name="OMF path textbook" /> there is rarely any pain.<ref name="Tyldesley 2003" /> Candida is associated with about 90% of cases of denture related stomatitis.<ref name="OMF medicine textbook" />

Median rhomboid glossitisEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} This is an elliptical or rhomboid lesion in the center of the dorsal tongue, just anterior (in front) of the circumvallate papillae. The area is depapillated, reddened (or red and white) and rarely painful. There is frequently Candida species in the lesion, sometimes mixed with bacteria.<ref name="Scully 2013" />

Linear gingival erythemaEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} This is a localized or generalized, linear band of erythematous gingivitis (inflammation of the gums). It was first observed in HIV infected individuals and termed "HIV-gingivitis", but the condition is not confined to this group.<ref name="Samaranayake 2009" /> Candida species are involved, and in some cases the lesion responds to antifungal therapy, but it is thought that other factors exist, such as oral hygiene and human herpesviruses. This condition can develop into necrotizing ulcerative periodontitis.<ref name="Newman 2012">Template:Cite book</ref>

OthersEdit

Chronic multifocal oral candidiasisEdit

This is an uncommon form of chronic (more than one month in duration) candidal infection involving multiple areas in the mouth, without signs of candidiasis on other mucosal or cutaneous sites. The lesions are variably red and/or white. Unusually for candidal infections, there is an absence of predisposing factors such as immunosuppression, and it occurs in apparently healthy individuals, normally elderly males. Smoking is a known risk factor.<ref name="Scully 2013" />

Chronic mucocutaneous candidiasisEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} This refers to a group of rare syndromes characterized by chronic candidal lesions on the skin, in the mouth and on other mucous membranes (i.e., a secondary oral candidiasis). These include Localized chronic mucocutaneous candidiasis, diffuse mucocutaneous candidiasis (Candida granuloma), candidiasis–endocrinopathy syndrome and candidiasis thymoma syndrome. About 90% of people with chronic mucocutaneous candidiasis have candidiasis in the mouth.<ref name="Greenberg 2008" />

Signs and symptomsEdit

Signs and symptoms are dependent upon the type of oral candidiasis. Often, apart from the appearance of the lesions, there are usually no other signs or symptoms. Most types of oral candidiasis are painless, but a burning sensation may occur in some cases.<ref name="Rhodus 2012" /> Candidiasis can, therefore, sometimes be misdiagnosed as burning mouth syndrome. A burning sensation is more likely with erythematous (atrophic) candidiasis, whilst hyperplastic candidiasis is normally entirely asymptomatic.<ref name="OMF path textbook" /> Acute atrophic candidiasis may feel like the mouth has been scalded with a hot liquid.<ref name="OMF path textbook" /> Another potential symptom is a metallic, acidic, salty or bitter taste in the mouth.<ref name="OMF path textbook" /><ref name="Rhodus 2012" /> The pseudomembranous type rarely causes any symptoms apart from possibly some discomfort or bad taste due to the presence of the membranes.<ref name="OMF path textbook" /><ref name="Greenberg 2008" /> Sometimes the patient describes the raised pseudomembranes as "blisters."<ref name="OMF path textbook" /> Occasionally there can be dysphagia (difficulty swallowing), which indicates that the candidiasis involves the oropharynx or the esophagus,<ref name="Bruch 2010" /> as well as the mouth. The trachea and the larynx may also be involved where there is oral candidiasis, and this may cause hoarseness of the voice.<ref name="Tyldesley 2003" />

CausesEdit

SpeciesEdit

The causative organism is usually Candida albicans,<ref name="OMF path textbook" /> or less commonly other Candida species such as (in decreasing order of frequency) Candida tropicalis,<ref name="Ghom 2010" /> Candida glabrata,<ref name="Ghom 2010" /> Candida parapsilosis,<ref name="Ghom 2010" /> Candida krusei,<ref name="Ghom 2010" /> or other species (Candida stellatoidea,<ref name="Ghom 2010" /> Candida pseudotropicalis,<ref name="Ghom 2010" /> Candida famata,<ref name="Ghom 2010" /> Candida rugosa,<ref name="Ghom 2010" /> Candida geotrichium,<ref name="Scully 2013" /> Candida dubliniensis,<ref name="Scully 2013" /> and Candida guilliermondii).<ref name="Ghom 2010">Template:Cite book</ref> C. albicans accounts for about 50% of oral candidiasis cases,<ref name="Williams 2011" /> and together C. albicans, C. tropicalis and C. glabrata account for over 80% of cases.<ref name="Greenberg 2008" /> Candidiasis caused by non-C. albicans Candida (NCAC) species is associated more with immunodeficiency.<ref name="Scully 2013" /> For example, in HIV/AIDS, C. dubliniensis and C. geotrichium can become pathogenic.<ref name="Scully 2013" />

About 35-50% of humans possess C. albicans as part of their normal oral microbiota.<ref name="OMF path textbook" /> With more sensitive detection techniques, this figure is reported to rise to 90%.<ref name="Greenberg 2008" /> This candidal carrier state is not considered a disease, since there are no lesions or symptoms of any kind. Oral carriage of Candida is pre-requisite for the development of oral candidiasis. For Candida species to colonize and survive as a normal component of the oral microbiota, the organisms must be capable of adhering to the epithelial surface of the mucous membrane lining the mouth.<ref name="Naglik 2011">Template:Cite journal</ref> This adhesion involves adhesins (e.g., hyphal wall protein 1), and extracellular polymeric materials (e.g., mannoprotein).<ref name="Scully 2013" /> Therefore, strains of Candida with more adhesion capability have more pathogenic potential than other strains.<ref name="Greenberg 2008" /> The prevalence of Candida carriage varies with geographic location,<ref name="Greenberg 2008" /> and many other factors. Higher carriage is reported during the summer months,<ref name="Greenberg 2008" /> in females,<ref name="Greenberg 2008" /> in hospitalized individuals,<ref name="Greenberg 2008" /> in persons with blood group O and in non-secretors of blood group antigens in saliva.<ref name="Greenberg 2008" /> Increased rates of Candida carriage are also found in people who eat a diet high in carbohydrates, people who wear dentures, people with xerostomia (dry mouth), in people taking broad spectrum antibiotics, smokers, and in immunocompromised individuals (e.g., due to HIV/AIDS, diabetes, cancer, Down syndrome or malnutrition).<ref name="Scully 2013" /> Age also influences oral carriage, with the lowest levels occurring in newborns, increasing dramatically in infants, and then decreasing again in adults. Investigations have quantified oral carriage of Candida albicans at 300-500 colony forming units in healthy persons.<ref name="Lynch 1994" /> More Candida is detected in the early morning and the late afternoon. The greatest quantity of Candida species are harbored on the posterior dorsal tongue,<ref name="Scully 2013" /> followed by the palatal and the buccal mucosae.<ref name="Lynch 1994" /> Mucosa covered by an oral appliance such as a denture harbors significantly more candida species than uncovered mucosa.<ref name="Lynch 1994" />

When Candida species cause lesions - the result of invasion of the host tissues - this is termed candidiasis.<ref name="OMF medicine textbook" /><ref name="Naglik 2011" /> Some consider oral candidiasis a change in the normal oral environment rather than an exposure or true "infection" as such.<ref name="Bruch 2010" /> The exact process by which Candida species switch from acting as normal oral commensals (saprophytic) state in the carrier to acting as a pathogenic organism (parasitic state) is not completely understood.<ref name="Greenberg 2008">Template:Cite book</ref>

Several Candida species are polymorphogenic,<ref name="Williams 2011" /> that is, capable of growing in different forms depending on the environmental conditions. C. albicans can appear as a yeast form (blastospores), which is thought to be relatively harmless; and a hyphal form associated with invasion of host tissues.<ref name="OMF path textbook" /> Apart from true hyphae, Candida can also form pseudohyphae — elongated filamentous cells, lined end to end.<ref name="Samaranayake 2009" /> As a general rule, candidiasis presenting with white lesions is mainly caused by Candida species in the hyphal form and red lesions by yeast forms.<ref name="Scully 2013" /> C. albicans and C. dubliniensis are also capable of forming germ tubes (incipient hyphae) and chlamydospores under the right conditions. C. albicans is categorized serologically into A or B serotypes. The prevalence is roughly equal in healthy individuals, but type B is more prevalent in immunocompromised individuals.Template:Cn

Predisposing factorsEdit

Common local and systemic predisposing factors.<ref name="Williams 2011" />
Local host factors
Systemic host factors

The host defenses against opportunistic infection of candida species are

  • The oral epithelium, which acts both as a physical barrier preventing micro-organisms from entering the tissues, and is the site of cell mediated immune reactions.
  • Competition and inhibition interactions between candida species and other micro-organisms in the mouth, such as the many hundreds of different kinds of bacteria.
  • Saliva, which possesses both mechanical cleansing action and immunologic action, including salivary immunoglobulin A antibodies, which aggregate candida organisms and prevent them adhering to the epithelial surface; and enzymatic components such as lysozyme, lactoperoxidase and antileukoprotease.<ref name="Scully 2013" />

Disruption to any of these local and systemic host defense mechanisms constitutes a potential susceptibility to oral candidiasis, which rarely occurs without predisposing factors.<ref name="Samaranayake 2009" /> It is often described as being "a disease of the diseased",<ref name="OMF medicine textbook" /><ref name="Samaranayake 2009" /> occurring in the very young, the very old, or the very sick.<ref name="Samaranayake 2009" /><ref name="Greenberg 2008" /><ref name="Scully 1994">Template:Cite journal</ref>

File:Thrush2010.JPG
Oral candidiasis in an infant. At very young ages, the immune system is yet to develop fully.

ImmunodeficiencyEdit

Immunodeficiency is a state of reduced function of the immune system, which can be caused by medical conditions or treatments.

Acute pseudomembranous candidiasis occurs in about 5% of newborn infants.<ref name="Soames 1999" /> Candida species are acquired from the mother's vaginal canal during birth. At very young ages, the immune system is yet to develop fully and there is no individual immune response to candida species,<ref name="Soames 1999" /> an infants antibodies to the fungus are normally supplied by the mother's breast milk.

Other forms of immunodeficiency which may cause oral candidiasis include HIV/AIDS,<ref name="Li 2013">Template:Cite journal</ref> active cancer and treatment, chemotherapy or radiotherapy.<ref name="Kerawala 2010" /><ref name="Epstein 2012">Template:Cite journal</ref>

Corticosteroid medications may contribute to the appearance of oral candidiasis,<ref name="Odell 2010" /> as they cause suppression of immune function either systemically or on a local/mucosal level, depending on the route of administration. Topically administered corticosteroids in the mouth may take the form of mouthwashes, dissolving lozenges or mucosal gels; sometimes being used to treat various forms of stomatitis. Systemic corticosteroids may also result in candidiasis.

Inhaled corticosteroids (e.g., for treatment of asthma or chronic obstructive pulmonary disease), are not intended to be administered topically in the mouth, but inevitably there is contact with the oral and oropharyngeal mucousa as it is inhaled. In asthmatics treated with inhaled steroids, clinically detectable oral candidiasis may occur in about 5-10% of adults and 1% of children.<ref name="Inhaledsteroids2001">Template:Cite book</ref> Where inhaled steroids are the cause, the candidal lesions are usually of the erythematous variety.<ref name="Greenberg 2008" /> Candidiasis appears at the sites where the steroid has contacted the mucosa, typically the dorsum of the tongue (median rhomboid glossitis) and sometimes also on the palate.<ref name=DaSilva2007 /><ref name="Lin2014">Template:Cite book</ref> Candidal lesions on both sites are sometimes termed "kissing lesions"<ref name=DaSilva2007>Template:Cite book</ref><ref name="Lin2014" /> because they approximate when the tongue is in contact with the palate.

Denture wearingEdit

Denture wearing and poor denture hygiene, particularly wearing the denture continually rather than removing it during sleep,<ref name="Kerawala 2010" /> is another risk factor for both candidal carriage and oral candidiasis. Dentures provide a relative acidic, moist and anaerobic environment because the mucosa covered by the denture is sheltered from oxygen and saliva.<ref name="Tarçın 2011" /> Loose, poorly fitting dentures may also cause minor trauma to the mucosa,<ref name="Samaranayake 2009" /> which is thought to increase the permeability of the mucosa and increase the ability of C. albicans to invade the tissues.<ref name="Tarçın 2011" /><ref name="Gendreau 2011">Template:Cite journal</ref> These conditions all favor the growth of C. albicans. Sometimes dentures become very worn, or they have been constructed to allow insufficient lower facial height (occlusal vertical dimension), leading to over-closure of the mouth (an appearance sometimes described as "collapse of the jaws"). This causes deepening of the skin folds at the corners of the mouth (nasolabial crease), in effect creating intertriginous areas where another form of candidiasis, angular cheilitis, can develop. Candida species are capable of adhering to the surface of dentures, most of which are made from polymethylacrylate. They exploit micro-fissures and cracks in the surface of dentures to aid their retention. Dentures may therefore become covered in a biofilm,<ref name="Williams 2011" /> and act as reservoirs of infection,<ref name="Bruch 2010" /> continually re-infecting the mucosa. For this reason, disinfecting the denture is a vital part of treatment of oral candidiasis in persons who wear dentures, as well as correcting other factors like inadequate lower facial height and fit of the dentures.

Dry mouthEdit

Both the quantity and quality of saliva are important oral defenses against candida.<ref name="Greenberg 2008" /> Decreased salivary flow rate or a change in the composition of saliva,<ref name="Rhodus 2012" /> collectively termed salivary hypofunction or hyposalivation is an important predisposing factor. Xerostomia is frequently listed as a cause of candidiasis,<ref name="Kerawala 2010" /> but xerostomia can be subjective or objective, i.e., a symptom present with or without actual changes in the saliva consistency or flow rate.

DietEdit

Malnutrition,<ref name="Kerawala 2010" /> whether by malabsorption,<ref name="Ghom 2010" /> or poor diet, especially hematinic deficiencies (iron, vitamin B12, folic acid) can predispose to oral candidiasis,<ref name="Greenberg 2008" /> by causing diminished host defense and epithelial integrity. For example, iron deficiency anemia is thought to cause depressed cell-mediated immunity.<ref name="Tarçın 2011" /> Some sources state that deficiencies of vitamin A or pyridoxine are also linked.<ref name="Ghom 2010" />

There is limited evidence that a diet high in carbohydrates predisposes to oral candidiasis.<ref name="Soames 1999" /> In vitro and studies show that Candidal growth, adhesion and biofilm formation is enhanced by the presence of carbohydrates such as glucose, galactose and sucrose.<ref name="Tarçın 2011" />

SmokingEdit

Smoking, especially heavy smoking, is an important predisposing factor but the reasons for this relationship are unknown. One hypothesis is that cigarette smoke contains nutritional factors for C. albicans, or that local epithelial alterations occur that facilitate colonization of candida species.<ref name="Tarçın 2011">Template:Cite journal</ref>

AntibioticsEdit

Broad-spectrum antibiotics (e.g. tetracycline) eliminate the competing bacteria and disrupt the normally balanced ecology of oral microorganisms,<ref name="OMF path textbook" /><ref name="Greenberg 2008" /> which can cause antibiotic-induced candidiasis.<ref name="Kerawala 2010" />

Other factorsEdit

Several other factors can contribute to infection, including endocrine disorders (e.g. diabetes when poorly controlled),<ref name="Rautemaa 2011">Template:Cite journal</ref> and/or the presence of certain other mucosal lesions, especially those that cause hyperkeratosis and/or dysplasia<ref name="Samaranayake 2009">Template:Cite book</ref> (e.g. lichen planus). Such changes in the mucosa predispose it to secondary infection with candidiasis.<ref name="Soames 1999">Template:Cite book</ref><ref name="Odell 2010" /> Other physical mucosal alterations are sometimes associated with candida overgrowth, such as fissured tongue (rarely),<ref name="Bruch 2010">Template:Cite book</ref> tongue piercing, atopy,<ref name="Greenberg 2008" /> and/or hospitalization.<ref name="Samaranayake 2009" />

DiagnosisEdit

The diagnosis can typically be made from the clinical appearance alone,<ref name="Bruch 2010" /> but not always. As candidiasis can be variable in appearance, and present with white, red or combined white and red lesions, the differential diagnosis can be extensive. In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen planus, oral hairy leukoplakia. Erythematous candidiasis can mimic geographic tongue. Erythematous candidiasis usually has a diffuse border that helps distinguish it from erythroplakia, which normally has a sharply defined border.<ref name="Greenberg 2008" />

Special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears.<ref name="Kumaraswamy 2012">Template:Cite journal</ref> Smears are collected by gentle scraping of the lesion with a spatula or tongue blade and the resulting debris directly applied to a glass slide. Oral swabs are taken if culture is required. Some recommend that swabs be taken from 3 different oral sites.<ref name="Kerawala 2010" /> Oral rinse involves rinsing the mouth with phosphate-buffered saline for 1 minute and then spitting the solution into a vessel that examined in a pathology laboratory. Oral rinse technique can distinguish between commensal candidal carriage and candidiasis. If candidal leukoplakia is suspected, a biopsy may be indicated.<ref name="Kumaraswamy 2012" /> Smears and biopsies are usually stained with periodic acid-Schiff, which stains carbohydrates in fungal cell walls in magenta. Gram staining is also used as Candida stains are strongly Gram positive.<ref name="Odell 2010">Template:Cite book</ref>

Sometimes an underlying medical condition is sought, and this may include blood tests for full blood count and hematinics.

If a biopsy is taken, the histopathologic appearance can be variable depending upon the clinical type of candidiasis. Pseudomembranous candidiasis shows hyperplastic epithelium with a superficial parakeratotic desquamating (i.e., separating) layer.<ref name="Purkait 2011">Template:Cite book</ref> Hyphae penetrate to the depth of the stratum spinosum,<ref name="Samaranayake 2009" /> and appear as weakly basophilic structures. Polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria.<ref name="Purkait 2011" />

Atrophic candidiasis appears as thin, atrophic epithelium, which is non-keratinized. Hyphae are sparse, and inflammatory cell infiltration of the epithelium and the lamina propria. In essence, atrophic candidiasis appears like pseudomembranous candidiasis without the superficial desquamating layer.<ref name="Purkait 2011" />

Hyperplastic candidiasis is variable. Usually there is hyperplastic and acanthotic epithelium with parakeratosis. There is an inflammatory cell infiltrate and hyphae are visible. Unlike other forms of candidiasis, hyperplastic candidiasis may show dysplasia.<ref name="Purkait 2011" />

TreatmentEdit

Oral candidiasis can be treated with topical anti-fungal drugs, such as nystatin, miconazole, Gentian violet or amphotericin B. Surgical excision of the lesions may be required in cases that do not respond to anti-fungal medications.<ref>Template:Cite journal</ref>

Underlying immunosuppression may be medically manageable once it is identified, and this helps prevent recurrence of candidal infections.

Patients who are immunocompromised, either with HIV/AIDS or as a result of chemotherapy, may require systemic prevention or treatment with oral or intravenous administered anti-fungals. However, there is strong evidence that drugs that are absorbed or partially absorbed from the GI tract can prevent candidiasis more effectively than drugs that are not absorbed in the same way.<ref>Template:Cite journal</ref>

If candidiasis is secondary to corticosteroid or antibiotic use, then use may be stopped, although this is not always a feasible option. Candidiasis secondary to the use of inhaled steroids may be treated by rinsing out the mouth with water after taking the steroid.<ref name="Tyldesley 2003" /> Use of a spacer device to reduce the contact with the oral mucosa may greatly reduce the risk of oral candidiasis.<ref name="Inhaledsteroids2001" />

In recurrent oral candidiasis, the use of azole antifungals risks selection and enrichment of drug-resistant strains of candida organisms.<ref name="Rautemaa 2011" /> Drug resistance is increasingly more common and presents a serious problem in persons who are immunocompromised.<ref name="Scully 2013" />

Prophylactic use of antifungals is sometimes employed in persons with HIV disease, during radiotherapy, during immunosuppressive or prolonged antibiotic therapy as the development of candidal infection in these groups may be more serious.<ref name="OMF medicine textbook" />

The candidal load in the mouth can be reduced by improving oral hygiene measures, such as regular toothbrushing and use of anti-microbial mouthwashes.<ref name="Williams 2011" /> Since smoking is associated with many forms of oral candidiasis, cessation may be beneficial.<ref name="Scully 2013"/>

Denture hygieneEdit

Template:See also Good denture hygiene involves regular cleaning of the dentures, and leaving them out of the mouth during sleep. This gives the mucosa a chance to recover, while wearing a denture during sleep is often likened to sleeping in one's shoes. In oral candidiasis, the dentures may act as a reservoir of Candida species known as denture stomatitis<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref name="Bruch 2010" /> which continually reinfects the mucosa once antifungal medication is stopped. Therefore, they must be disinfected as part of the treatment for oral candidiasis. There are commercial denture cleaner preparations for this purpose, but it is readily accomplished by soaking the denture overnight in a 1:10 solution of sodium hypochlorite (Milton, or household bleach).<ref name="Bruch 2010" /> Bleach may corrode metal components,<ref name="Scully 2013" /> so if the denture contains metal, soaking it twice daily in chlorhexidine solution can be carried out instead. An alternative method of disinfection is to use a 10% solution of acetic acid (vinegar) as an overnight soak, or to microwave the dentures in 200mL water for 3 minutes at 650 watts.<ref name="Scully 2013">Template:Cite book</ref> Microwave sterilization is only suitable if no metal components are present in the denture. Antifungal medication can also be applied to the fitting surface of the denture before it is put back in the mouth. Other problems with the dentures, such as inadequate occlusal vertical dimension may also need to be corrected in the case of angular cheilitis.

PrognosisEdit

The severity of oral candidiasis is subject to great variability from one person to another and in the same person from one occasion to the next.<ref name="Rhodus 2012" /> The prognosis of such infection is usually excellent after the application of topical or systemic treatments. However, oral candidiasis can be recurrent.<ref name="Rhodus 2012" /> Individuals continue to be at risk of the condition if underlying factors such as reduced salivary flow rate or immunosuppression are not rectifiable.<ref name="Rhodus 2012" />

Candidiasis can be a marker for underlying disease,<ref name="Lynch 1994" /> so the overall prognosis may also be dependent upon this. For example, a transient erythematous candidiasis that developed after antibiotic therapy usually resolves after antibiotics are stopped (but not always immediately),<ref name="Tyldesley 2003" /> and therefore carries an excellent prognosis—but candidiasis may occasionally be a sign of more sinister undiagnosed pathology, such as HIV/AIDS or leukemia.

It is possible for candidiasis to spread to/from the mouth, from sites such as the pharynx, esophagus, lungs, liver, anogenital region, skin or the nails.<ref name="Scully 2013" /> The spread of oral candidiasis to other sites usually occurs in debilitated individuals.<ref name="Tyldesley 2003" /> It is also possible that candidiasis is spread by sexual contact.<ref name="Scully 2013" /> Rarely, a superficial candidal infection such as oral candidiasis can cause invasive candidiasis, and even prove fatal. The observation that Candida species are normally harmless commensals on the one hand, but are also occasionally capable of causing fatal invasive candidiases, has led to the description "Dr Jekyll and Mr Hyde".<ref name="Gow 2002">Template:Cite journal</ref>

The role of thrush in the hospital and ventilated patients is not entirely clear, however, there is a theoretical risk of positive interaction of candida with topical bacteria.<ref name="Peleg_2010">Template:Cite journal</ref>

EpidemiologyEdit

In humans, oral candidiasis is the most common form of candidiasis,<ref name="Ghom 2010" /> by far the most common fungal infection of the mouth,<ref name="OMF path textbook">Template:Cite book</ref> and it also represents the most common opportunistic oral infection in humans<ref name="Lalla 2013">Template:Cite journal</ref> with lesions only occurring when the environment favors pathogenic behavior.

Oropharyngeal candidiasis is common during cancer care,<ref name="Epstein 2012" /> and it is a very common oral sign in individuals with HIV.<ref name="Li 2013" /> Oral candidiasis occurs in about two thirds of people with concomitant AIDS and esophageal candidiasis.<ref name="Yamada 2009">Template:Cite book</ref>

The incidence of all forms of candidiasis have increased in recent decades. This is due to developments in medicine, with more invasive medical procedures and surgeries, more widespread use of broad spectrum antibiotics and immunosuppression therapies. The HIV/AIDs global pandemic has been the greatest factor in the increased incidence of oral candidiasis since the 1980s. The incidence of candidiasis caused by NCAC species is also increasing, again thought to be due to changes in medical practise (e.g., organ transplantation and use of indwelling catheters).<ref name="Williams 2011" />

HistoryEdit

Oral candidiasis has been recognized throughout recorded history.<ref name="Williams 2011">Template:Cite journal</ref> The first description of this condition is thought to have occurred in the 4th century B.C. in "Epidemics" (a treatise that is part of the hippocratic corpus), where descriptions of what sounds like oral candidiasis are stated to occur with severe underlying disease.<ref name="Lynch 1994">Template:Cite journal</ref><ref name=ID10>Template:Cite book</ref>

The colloquial term "thrush" is of unknown origin but may stem from an unrecorded Old English word *þrusc or from a Scandinavian root. The term is not related to the bird of the same name.<ref> “Thrush, N. (2).” Oxford English Dictionary, Oxford UP, July 2023, https://doi.org/10.1093/OED/1201547560.</ref>

Society and cultureEdit

Many pseudoscientific claims by proponents of alternative medicine surround the topic of candidiasis. Oral candidiasis is sometimes presented in this manner as a symptom of a widely prevalent systemic candidiasis, candida hypersensitivity syndrome, yeast allergy, or gastrointestinal candida overgrowth, which are medically unrecognized conditions. Template:Cn(See: Alternative medicine in Candidiasis)

ReferencesEdit

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External linksEdit

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