Denture stomatitis is a common oral mucosal lesion in the United States and Western Europe. Prevalence rates of 2.5-18.3% in adults aged 35-44 years or 65-74 years are reported, with a predominance in the latter age group.[1, 2] Although patient age and denture quality alone do not predispose individuals this mucosal condition, the odds of developing stomatitis, denture-related hyperplasia, and angular cheilitis are increased almost 3-fold in denture wearers.[3] Studies indicate that correlations may exist with the amount of tissue coverage by a maxillary denture, vitamin A levels, smoking of cigarettes, and not removing dentures.[4]
Mucosal factors have been implicated in the etiology of this condition, as have behavioral and manner-of-use factors in patients who wear complete dentures. In these patients, the nighttime wear of the prosthetic appliance is the most significant factor.[5, 6]
Although the dominant etiologic factor now appears to be fungal infection, other factors must be considered; these include the prosthetic device itself and also local and systemic factors in patients who are aging and edentulous. The extent of inflammation has been correlated with the presence of yeast colonizing the denture surface.[7] Trauma has been shown to have a role in the production of basement membrane alterations involving expression of type IV collagen and laminin (alpha 1), thus indicating a possible relationship between these elements and denture stomatitis.[8] Regarding the prosthesis-related factor, an allergy in the form of contact mucositis is suggested. This reaction may be related to the presence of resin monomers, hydroquinone peroxide, dimethyl-p -toluidine, or methacrylate in the denture. Furthermore, contact sensitivities such as this one are more common with cold or autocured resins than with heat-cured denture-base materials.
Candida species have been identified in most patients[9, 10] or in all patients,[11] with Candida albicans being the predominant species isolated in addition to many other candidal species.[12] Whether the organism is merely commensal in this situation remains an issue because of the frequency of such organisms in the general population; the role of this organism as the sole etiologic factor in denture stomatitis is unclear; however, the presence of candidal organisms within the overall biofilm lends credence to its role in the development and maintenance of denture stomatitis.[13] The etiology is best considered multifactorial, with the prosthesis considered the prime etiologic factor. The character of biofilm communities of denture wearers, however, has been shown to be distinctive when compared with healthy non – denture-wearing individuals.[14]
Related Medscape Reference articles include Noncandidal Fungal Infections of the Mouth and Mucosal Candidiasis.
The exact prevalence of denture stomatitis is unknown, but it appears to be 2.5-18.3% among adults. The disease is common in elderly persons, especially those living in nursing home facilities. Findings from several studies suggest that denture stomatitis develops in as many as 35-50% of persons who wear complete dentures.[15, 16]
International
Denture stomatitis is a common oral mucosal lesion in Western Europe, Thailand, and Turkey.[17, 18]
Race
No racial predilection is recognized.
Sex
Sex-related frequencies differ among studies; therefore, no clear sex predilection is apparent.
Age
The disease is more common in elderly persons than in young persons because elderly persons are more likely to wear dentures and because their level of oral and denture hygiene is reduced. In addition, age-related chronic disease (eg, type 2 diabetes mellitus), iatrogenic drugs, and age-associated immunocompromise contribute to this risk level.
Denture stomatitis usually occurs in a patient who wears a complete maxillary denture or a partial denture. The presence of deteriorating temporary soft denture lining material and an improperly matched cleanser (which generally is the case) is associated with an increased presence of candidal organisms within the biofilm.[19, 20]
In almost all patients, the duration of the lesion is usually unknown because of its asymptomatic nature.
On rare occasions, patients may complain of slight bleeding and swelling in the involved area, as well as a burning sensation, a xerostomialike quality, or cacogeusia.[21]
Although symptoms are uncommon, the clinical presentation of erythema and edema in the part of the palatal mucosa covered by the denture base is a diagnostic finding. Intense erythema is the most common finding. Note the image below.
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A variably intense erythema distributed over the part of the mucosa covered by the denture base is diagnostic of denture stomatitis.
At times, an obvious fungal infection in the form of white surface colonies or plaques may be observed on the mucosal surface. Variably intense erythema, which may also be associated with scattered petechiae, is distributed over the mucosa covered by the base of the denture but not beyond. Palpation of the involved mucosa reveals no tenderness or tissue friability. The severity of denture stomatitis can vary (see Staging).
A smear of the fungal material from the mucosa can be prepared and studied by using a potassium hydroxide (KOH) preparation or periodic acid-Schiff staining in the laboratory. Other methods of identifying fungal organisms involve the use of imprint cultures.[22]
Inflammatory papillary epithelial hyperplasia (IPEH) is not associated with cytologic signs of dysplasia. Epithelial dysplasia has not been observed in specimens of denture stomatitis.
The level of denture stomatitis can be classified as follows[23] :
Type I - Pinpoint hyperemia or localized simple inflammation
Type II - Diffuse erythema confined to the mucosa in contact with the denture base (see image below)
View Image
A variably intense erythema distributed over the part of the mucosa covered by the denture base is diagnostic of denture stomatitis.
Type III - Granular surface or inflammatory papillary hyperplasia of the palate (see image below)
View Image
When untreated and chronic, papillary epithelial hyperplasia may develop. This may need to be surgically removed before the denture is replaced or rel....
Type III denture stomatitis involves the epithelial response to chronic inflammatory stimulation secondary to yeast colonization and, possibly, low-grade local trauma resulting from an ill-fitting denture.
Mechanical plaque control and appropriate denture-wearing habits are the most important measures in preventing and treating the disease. Also, denture sanitization is an important element in the treatment of denture stomatitis.
Despite the absence of symptoms, patients with advanced, chronic, or previously untreated cases must be treated because of the risk of papillary epithelial hyperplasia. IPEH usually needs to be surgically removed before the denture is emplaced or relined. In mild cases of IPEH, antifungal treatment without surgery might be an alternative before the dentures are relined or replaced.
In the absence of papillary hyperplasia, verify denture-base adaptation to the alveolar and palatal mucosal surfaces and identify and correct occlusal disharmonies, vertical dimension, and centric position. Scrupulous denture hygiene is mandatory, with daily thorough brushing. The dentures should be soaked overnight in an antiseptic solution such as chlorhexidine or dilute sodium hypochlorite (10 drops of household bleach in a denture cup or container filled with tap water). If the denture base contains metal, the patient should avoid using hypochlorite because it causes metal to tarnish. Another benefit of the regimen of overnight denture soaking is that the patients must remove their dentures for a prolonged period. Removal of the denture minimizes additional irritation and is a cornerstone of treatment.[24]
Initiate antifungal therapy if fungal organisms are identified or if the condition fails to resolve even with the regimen described above. Topical therapy is the first-line treatment. The use of clotrimazole or nystatin lozenges and/or pastilles, with the denture removed from the mouth, is recommended. The application of antifungal agents (eg, nystatin powder or cream) on the tissue-contacting surface of the denture is also recommended. Combine topical medical treatment with proper care of the denture, as described above.
In cases that fail to respond to the usual treatments, consider the role of systemic disease and its impact on oral function and homeostasis. Chief among the systemic conditions that may affect denture stomatitis is type 2 diabetes mellitus. In patients with type 2 diabetes mellitus, the number of candidal organisms that adhere to the palatal epithelial cells is significantly increased; this finding supports the notion that this form of diabetes predisposes patients to Candida -associated denture stomatitis. However, a recent study group suggested that reduced resistance to candidal organisms preset before the development of type 2 diabetes mellitus is related to denture stomatitis.[25]
Other conditions that may need to be excluded include cellular immunodeficiency and humoral immunologic disorders, HIV infection, hypothyroidism, poor diet, and iatrogenic drug use.[26]
A study evaluated the in vitro antifungal activity of apple cider vinegar on Candida spp. involved in denture stomatitis. The study concluded that apple cider vinegar showed antifungal properties against Candida spp., thus representing a possible therapeutic alternative for patients with denture stomatitis.[27]
Clinical Context:
Fungicidal and fungistatic antibiotic obtained from Streptomyces noursei; effective against various yeasts and yeastlike fungi. Changes permeability of fungal cell membrane after binding to cell membrane sterols, causing cellular contents to leak. Treatment should continue until 48 h after symptoms disappear. Reevaluate after 14 days of treatment if no improvement. Drug is not significantly absorbed from GI tract.
Mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell. It may also involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.
Clinical Context:
This agent adheres to the mucosal surface of mouth and forms a protective coating that shields exposed and overstimulated nerve endings. Ingredients include water, maltodextrin, propylene glycol, polyvinylpyrrolidone (PVP), sodium hyaluronate, potassium sorbate, sodium benzoate, hydroxy ethylcellulose, polyethylene glycol (PEG)–40, hydrogenated castor oil, disodium edetate, benzalkonium chloride, flavoring, saccharin sodium, and glycyrrhetinic acid.
Denture sanitization is an important element in the treatment of denture stomatitis and should be emphasized to the patients. The 6-month incidence of denture stomatitis can be significantly reduced by educating nursing home caregivers about oral heath care.
The incidence of denture stomatitis and the duration of denture wear are highly correlated. Dentists can help prevent this condition by instructing patients to take their dentures out of their mouth for 6-8 hours each day.
Mechanical plaque control and appropriate denture-wearing habits are the most important measures in preventing and treating the disease.
In most patients, the elimination of mechanical and traumatic factors, the consistent use of oral hygiene measures, and the administration of local antimycotic therapy usually enables the inflammatory lesions to heal rapidly.
Recurrences are common when exacerbating factors are reintroduced.
The need for an educational component in a preventive oral health care program in geriatric institutions is unmet.[28] Dental professionals who work with geriatric patients should address this need by implementing a preventive oral health care program. Such programs should include not only patient examinations and preventive care but also education for allied health care professionals and members of the patient's family.
Patients should be taught how to properly wear and sanitize their dentures and about how to perform good oral hygiene (see Deterrence/Prevention).
James J Sciubba, DMD, PhD, Consultant, The Milton J Dance Head and Neck Center, Greater Baltimore Medical Center; Private Practice in Oral Medicine/Oral Pathology; Professor (Ret) of Otolaryngology-Head and Neck Surgery, Professor of Pathology, Professor of Dermatology, Johns Hopkins School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Michael J Wells, MD, FAAD, Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology
Disclosure: Nothing to disclose.
Drore Eisen, MD, DDS, Consulting Staff, Dermatology of Southwest Ohio
Disclosure: Nothing to disclose.
Chief Editor
Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Peter Fritsch, MD Chair, Department of Dermatology and Venereology, University of Innsbruck, Austria
Peter Fritsch, MD is a member of the following medical societies: American Dermatological Association, International Society of Pediatric Dermatology, and Society for Investigative Dermatology
A variably intense erythema distributed over the part of the mucosa covered by the denture base is diagnostic of denture stomatitis.
A variably intense erythema distributed over the part of the mucosa covered by the denture base is diagnostic of denture stomatitis.
When untreated and chronic, papillary epithelial hyperplasia may develop. This may need to be surgically removed before the denture is replaced or relined.
A variably intense erythema distributed over the part of the mucosa covered by the denture base is diagnostic of denture stomatitis.
When untreated and chronic, papillary epithelial hyperplasia may develop. This may need to be surgically removed before the denture is replaced or relined.
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