to hiv/aids, diabetes, cancer, down syndrome or malnutrition). 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. 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, followed by the palatal and the buccal mucosae. mucosa covered by an oral appliance such as a denture harbors significantly more candida species than uncovered mucosa. when candida species cause lesions - the result of invasion of the host tissues - this is termed candidiasis. some consider oral candidiasis a change in the normal oral environment rather than an exposure or true "infection" as such. 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. several candida species are polymorphogenic, 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. apart from true hyphae, candida can also form pseudohyphae — elongated filamentous cells, lined end to end. 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. 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. predisposing factors common local and systemic predisposing factors. local host factors dentures corticosteroid inhalers reduced salivary flow high sugar diet systemic host factors extremes of age endocrine disorders (e.g., diabetes) immunosuppression broad spectrum antibiotics (e.g., tetracycline) nutritional deficiencies 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. disruption to any of these local and systemic host defense mechanisms constitutes a potential susceptibility to oral candidiasis, which rarely occurs without predisposing factors. it is often described as being "a disease of the diseased", occurring in the very young, the very old, or the very sick. oral candidiasis in an infant. at very young ages, the immune system is yet to develop fully. immunodeficiency 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. 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, 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, active cancer and treatment, chemotherapy or radiotherapy. corticosteroid medications may contribute to the appearance of oral candidiasis, 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. where inhaled steroids are the cause, the candidal lesions are usually of the erythematous variety. 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. candidal lesions on both sites are sometimes termed "kissing lesions" because they approximate when the tongue is in contact with the palate. denture wearing denture wearing and poor denture hygiene, particularly wearing the denture continually rather than removing it during sleep, 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. loose, poorly fitting dentures may also cause minor trauma to the mucosa, which is thought to increase the permeability of the mucosa and increase the ability of c. albicans to invade the tissues. 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, and act as reservoirs of infection, 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 mouth both the quantity and quality of saliva are important oral defenses against candida. decreased salivary flow rate or a change in the composition of saliva, collectively termed salivary hypofunction or hyposalivation is an important predisposing factor. xerostomia is frequently listed as a cause of candidiasis, but xerostomia can be subjective or objective, i.e., a symptom present with or without actual changes in the saliva consistency or flow rate. diet malnutrition, whether by malabsorption, or poor diet, especially hematinic deficiencies (iron, vitamin b12, folic acid) can predispose to oral candidiasis, by causing diminished host defense and epithelial integrity. for example, iron deficiency anemia is thought to cause depressed cell-mediated immunity. some sources state that deficiencies of vitamin a or pyridoxine are also linked. there is limited evidence that a diet high in carbohydrates predisposes to oral candidiasis. 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. smoking 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. antibiotics broad-spectrum antibiotics (e.g. tetracycline) eliminate the competing bacteria and disrupt the normally balanced ecology of oral microorganisms, which can cause antibiotic-induced candidiasis. other factors several other factors can contribute to infection, including endocrine disorders (e.g. diabetes when poorly controlled), and/or the presence of certain other mucosal lesions, especially those that cause hyperkeratosis and/or dysplasia (e.g. lichen planus). such changes in the mucosa predispose it to secondary infection with candidiasis. other physical mucosal alterations are sometimes associated with candida overgrowth, such as fissured tongue (rarely), tongue piercing, atopy, and/or hospitalization. diagnosis the diagnosis can typically be made from the clinical appearance alone, 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. special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears. 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. 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. 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. 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. hyphae penetrate to the depth of the stratum spinosum, and appear as weakly basophilic structures. polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria. 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. 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. treatment 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. 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. 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. use of a spacer device to reduce the contact with the oral mucosa may greatly reduce the risk of oral candidiasis. in recurrent oral candidiasis, the use of azole antifungals risks selection and enrichment of drug-resistant strains of candida organisms. drug resistance is increasingly more common and presents a serious problem in persons who are immunocompromised. 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. the candidal load in the mouth can be reduced by improving oral hygiene measures, such as regular toothbrushing and use of anti-microbial mouthwashes. since smoking is associated with many of forms of oral candidiasis, cessation may be beneficial. denture hygiene