Interrelationship between Candida Colonization, Dentures, and Mucosal Tissue Inflammation in the Pathogenesis of Denture Stomatitis

ABSTRACT

Despite being common, the pathogenesis of denture stomatitis (DS) is poorly known; thus, this study was conducted to examine the relationship between candida, dentures, and mucosal tissue inflammation. One hundred and twenty edentulous patients wearing a denture with clinical signs and symptoms of DS and 30 patients without DS as healthy were involved in the study. Patients with DS were divided into three groups according to Newton’s classification and fungal colonies, and denture fit was assessed. No significant difference was observed between age, sex, and denture fit between the two groups (P > 0.05). The fungal colonies in patients with DS were significantly more than the controls. The majority of the patients with good denture fit had degree 1 (localized mucosal inflammation), while the majority of the patients with fair denture fit had degree 2 (diffuse inflammation on the denture bearing area) and the majority with poor denture fit had degree 3 (granular type) (P < 0.001). The fungal colonies were negative for the majority of degree 1 patients (57.1%), while they were positive for the majority of patients with degree 2 (61.3%) and degree 3 (63.2%) inflammation (P = 0.003). We concluded that the pathogenesis of DS is elusive. Multiple factors, including lack of hygiene, reduced salivary flow, poor denture care, and fit, provide an easy pathway for Candida strains to colonize dentures.

INTRODUCTION

Denture stomatitis (DS) is an inflammation of the oral mucosa that most commonly involves gingival and palatal mucosa, which directly contacts the denture base. It occurs between 25 and 67% of the time, primarily in women, and its prevalence increases with age.[1,2]

Despite being common, the pathogenesis of DS is poorly known. Multiple etiological factors contribute to DS. These include 1) impaired salivary flow and salivary gland function; 2) fungal infection such as Candida albicans and gram-negative anaerobes; 3) ill-fitting prosthesis that results in trauma; 4) poor oral and denture hygiene; and 5) decreased immunity due to systemic conditions.[3,4]

However, for the most part, clear links between causes and effects have not been found between the associated etiologic factors. It is currently believed that DS is caused by multiple factors. It has been proposed that xerostomia, which is frequently but not always linked to reduced salivary flow or altered protein and inorganic composition of saliva, causes a change in the composition of the oral microbiome that encourages fungal growth. According to a theory, the interaction between salivary flow and viscosity may affect the epithelium resistance to Candida adhesion and invasion, contributing to DS.[5,6]

Poorly fitting dentures and an atrophic osseous ridge anatomy are usually linked to DS. It is unclear whether the inflammatory state of DS causes ridge resorption, resulting in a loose and easily removed denture, or whether the trauma associated with the denture (caused, e.g., by inadequate inter-ridge space, poor tissue adaptation, or clenching) results in mechanical stress that causes mucosal inflammation and bone resorption due to inadequate tissue perfusion, necrosis, or trauma. Other than this, patients who have poor oral hygiene, poor denture care, or who wear their dentures all night may find that their dentures exist as a breeding ground for high-density biofilm, which can contain a lot of bacteria and yeast.[4]

Although several studies have examined these DS etiologic factors, the majority of these studies emphasize just a handful of factors. DS can develop in a healthy person wearing a denture. Consequently, this study aimed to examine the relationship between candida, dentures, and mucosal tissue inflammation.

MATERIALS AND METHODS

Ethical approval has been obtained from the Institutional Ethical Committee (IEC) of Dasmesh Institute of Research and Dental Sciences, Faridkot, Punjab, India.

Source of the data

The study was conducted on 150 patients with or without DS visiting the Dasmesh Institute of Research and Dental Sciences, Faridkot, Punjab, India.

Selection criteria

One hundred and twenty edentulous patients wearing a denture with clinical signs and symptoms of DS and 30 patients without DS as healthy controls were involved in the study. Written informed consent was obtained from all study participants.

Patients with clinical signs and symptoms of DS and healthy controls without any visible signs and symptoms of DS were included in the study.

Subjects using antifungal or antibacterial antibiotics, those with overt denture abrasion coupled with symptoms, and those with chronic diseases with oral manifestations other than DS or mucosal stomatitis were excluded from the study.

Method of collection of data

Clinical evaluation of dentures (Kapur Index)

Using the Kapur Index, the maxillary and mandibular dentures’ fit was evaluated as either clinically poor (sum score less than 3), clinically fair (sum score between 3 and 4), or clinically good (sum score greater than 4).

Culture

A total of three swabs were obtained from the denture, the mucosal surface of the affected area, and the unaffected area for the disease group, and two swabs were taken from the denture and the mucosal surface for the control group. Swabs were used to collect samples, which were then grown on Sabouraud dextrose agar with kemicetine succinate. After 48 hours, Candida colonies were enumerated, and the patients were categorized as negative (colony-forming unit (CFU)/ml = 0), carrier (CFU/ml less than 400), and positive (CFU/ml greater than 400) based on the quantity of CFUs.

Patients with DS were divided into three groups according to Newton’s[7] classification.

Type I: localized mucosal inflammation mainly because of trauma.

Type II: diffuse inflammation of the denture bearing area.

Type III: granular.

The results were compiled in Microsoft (MS) Excel, and the statistical analysis was performed using Statistical Package for the Social Sciences (SPSS) version 26. An independent-samples t-test was used for grouped variables, and for categorical variables, the Chi-square test was performed. The P value < 0.05 was taken as significant, while <0.001 was taken as highly significant.

RESULTS

Table 1 shows study characteristics, which showed no significant difference between age, sex, and denture fit between the two groups (P > 0.05). The fungal colonies in patients with DS were significantly more than the controls.

Table 1.

Study characteristics (age, gender, denture fit, and Candida colonies)

Parameters	Group		P
	Cases	Control
Age (mean/SD)	64.79 (10.309)	66.87 (12.303)	0.34 (t-test)
Sex (n %)
Male	45 (37.5%)	10 (33.3%)	0.67
Female	75 (62.5%)	20 (66.7%)
Denture fit (n %)
Good denture	34 (28.3%)	11 (36.7%)	0.49
Fair denture	55 (45.8%)	14 (46.7%)
Poor denture	31 (25.8%)	5 (16.7%)
Fungal colonies (n %)
Negative (CFU/ml=0)	30 (25.0%)	14 (46.7%)	<0.001
Carrier (CFU/ml <400)	25 (20.8%)	13 (43.3%)
Positive (CFU/ml >400)	65 (54.2%)	3 (10.0%)

In Table 2, on comparing sex with degree of inflammation, it was observed that no significant difference was seen, and we observed that the majority of patients (66.7%) with good denture fit had degree 1 (localized mucosal inflammation), while the majority of patients with fair denture fit (53.8%) had degree 2 (diffuse inflammation on the denture bearing area) and the majority with poor denture fit (52.6%) had degree 3 (granular type) (P < 0.001).

Table 2.

Study characteristics in relation to different degrees of denture stomatitis

Variables	Degree 1		Degree 2		Degree 3		P
	n	%	n	%	n	%
Sex
Male	8	38.1%	32	40.0%	5	26.3%	0.540
Female	13	61.9%	48	60.0%	14	73.7%
Denture fit
Good	14	66.7%	18	22.5%	2	10.5%	<0.001
Fair	5	23.8%	43	53.8%	7	36.8%
Poor	2	9.5%	19	23.8%	10	52.6%
Fungal colonies
Negative (CFU/ml=0)	12	57.1%	16	20.0%	2	10.5%	0.003
Carrier (CFU/ml <400)	5	23.8%	15	18.8%	5	26.3%
Positive (CFU/ml >400)	4	19.0%	49	61.3%	12	63.2%

The fungal colonies were negative for the majority of degree one patients (57.1%), while they were positive for the majority of patients with degree 2 (61.3%) and degree 3 (63.2%) inflammation (P = 0.003).

DISCUSSION

The present study was conducted to determine the relationship between candida, dentures, and mucosal tissue. We found that the patients who had a higher degree of stomatitis had more fungal colonies and the denture fit also affected the degree of mucosal inflammation with patients with less inflammation having a better fit.

In their study, Budtz-Jorgensen and Bertram[8] observed a correlation between Newton’s grade and ill-fitting dentures, as well as the resulting irritation and trauma. Others have reported that ill-fitting dentures are associated with an increased risk of DS. Poor hygiene and Candida infection were found to be more significantly linked to more severe forms of stomatitis characterized by granular inflammation. Similar results were reported by Gendreau and Loewy.[9]

Candidal species, particularly C. albicans, are frequently found on the dentures and oral mucosa of people without DS symptoms.[10,11] In the present study, 43.30% of the controls were carriers, while 10% were positive for Candida albicans.

Candida, specifically C. albicans, is widely recognized as a significant etiological factor in DS due to its association with pathogenic Candida proliferation on denture surfaces and the oral mucosa. It has been determined that the presence of Candida correlates with the development of DS.[12] In our study, the fungal colonies were negative for the majority of degree 1 patients (57.1%), while they were positive for the majority of patients with degree 2 (61.3%) and degree 3 (63.2%) inflammation (P = 0.003).

In patients with DS, Budtz-Jorgensen and Bertram observed a substantial correlation between yeast colonization and inflammation in their 1970 publication; this correlation has been supported by additional research studies.

After wearing the denture, oral microbes shift, which stimulates the growth of organisms that cause DS. Bacterial contact and Candida albicans have been proven to be important causes of DS. Trauma has been found to cause Newton’s type I, whereas multivariable interaction phenomena cause Newton’s class III.[13,14]

Many people who wear complete dentures experience DS. Its etiology is complex. Poor denture fit and C. albicans colonization of the oral mucosa, particularly the mucosa in contact with denture fitting surfaces, are important risk factors for DS.

CONCLUSION

Multiple factors, including lack of hygiene, reduced salivary flow, poor denture care, and fit, provide pathways for Candida strains in colonizing dentures. Dentists must provide denture users with high-quality prosthetics and clear instructions on the significance of meticulous maintenance and the usage of a daily cleaning routine.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.