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Journal of Oral Biology and Craniofacial Research logoLink to Journal of Oral Biology and Craniofacial Research
. 2026 Aug 17;16(4):101504. doi: 10.1016/j.jobcr.2026.101504

Assessment of oral health, salivary alterations, and parental KAP in children with congenital heart disease

Kavita Dhinsa a, Brinda Suhas Godhi b, Sonali Saha c,⁎, Ayushi Singh d, Arunima Sarkar c, Antra Singh c
PMCID: PMC13540657  PMID: 42694697

Abstract

Background

Children with congenital heart disease (CHD) are at high risk for infective endocarditis (IE), with poor oral health being a key portal for bacteraemia. Data holistically integrating clinical status, salivary defence mechanisms, and parental behaviors in this vulnerable population are scarce.

Aim

To compare the oral health status, salivary parameters, Streptococcus mutans levels, and parental knowledge-attitude-practice (KAP) between children with CHD at risk for IE and healthy controls.

Materials and methods

This cross-sectional comparative study enrolled 65 children with IE-risk CHD and 65 age- and sex-matched healthy controls (aged 3-12 years). Assessments included the DMFT/deft and Simplified Oral Hygiene Index (OHI-S). Unstimulated saliva was analyzed for flow rate, pH, buffering capacity, viscosity, osmolality, and secretory IgA. S. mutans was quantified via culture. Parental KAP was evaluated using a validated questionnaire.

Results

The CHD group had significantly higher mean DMFT (4.2 ± 2.1 vs. 1.8 ± 1.5; p < 0.001) and OHI-S scores (2.5 ± 0.7 vs. 1.2 ± 0.5; p < 0.001). They exhibited compromised salivary function (reduced flow, pH, buffering, sIgA; p < 0.05) and elevated pathogenic markers (viscosity, osmolality, S. mutans counts >105 CFU/mL; p < 0.001). Parental KAP scores were significantly lower in the CHD group (p < 0.001). Regression analysis identified CHD status (β = 2.1, p < 0.001), low salivary flow (β = −0.8, p = 0.002), high S. mutans (β = 0.5, p = 0.01), and poor parental practice (β = −0.3, p = 0.03) as key predictors of caries severity.

Conclusion

Children with CHD exhibit a deleterious triad of severe caries, dysfunctional salivary defences, and inadequate parental preventive practices. These findings mandate the integration of point-of-care oral screening and structured parent education into routine cardiac follow-up to mitigate IE risk.

Keywords: Congenital heart disease, Infective endocarditis, Oral health, Streptococcus mutans, Salivary parameters

1. Introduction

Congenital Heart Disease (CHD) is one of the most prevalent developmental anomalies worldwide, affecting approximately 8-12 per 1000 live births, with a higher incidence in developing countries, such as India.1,2 These children often require prolonged medical management, including medications with acidic properties and fermentable carbohydrates, to enhance compliance, which can adversely impact oral health by lowering intraoral pH and promoting cariogenic environments.3 Oral health challenges are particularly pronounced in young patients with CHD, as their medical complexities may overshadow routine dental care, leading to increased susceptibility to dental caries, gingival diseases, and enamel defects.4 Moreover, poor oral hygiene in this population exacerbates the risk of bacteraemia from oral microorganisms, notably Streptococcus mutans, which is implicated in the pathogenesis of infective endocarditis (IE), a potentially life-threatening complication in individuals with cardiac defects.5,6

The interplay between oral health and systemic conditions in children with CHD is multi-faceted. Inadequate oral hygiene during daily activities, such as mastication or brushing, can introduce transient bacteremia and increase the risk of IE.7 Risk factors include frequent intake of sugared medications, developmental enamel hypoplasia, and prioritization of parental cardiac care over oral hygiene.7,8 Additionally, medication-induced xerostomia and alterations in salivary composition, such as reduced flow rate, pH, buffering capacity, and levels of protective components such as calcium, phosphorus, and immunoglobulin A (IgA), further contribute to elevated caries prevalence.3,8 Studies have shown that salivary hypofunction diminishes the natural defenses of the oral cavity, fostering microbial proliferation and demineralization.3,8 Despite these vulnerabilities, oral health assessments in children with CHD are often overlooked, underscoring the need for integrated pediatric dental and cardiac care.

Parental knowledge, attitudes, and practices (KAP) play a pivotal role in mitigating these risks. Parents of children with CHD may exhibit heightened awareness of IE prophylaxis. However, they often lack a comprehensive understanding of preventive oral health measures, leading to irregular dental visits and suboptimal hygiene routines.9 Limited studies from India highlight gaps in parental education, with many caregivers being unaware of the direct link between oral infections and cardiac complications. This neglect can perpetuate a cycle of poor oral health, emphasizing the importance of evaluating KAP along with clinical parameters to inform targeted interventions.

Therefore, the aim of this study was to evaluate and compare caries index, oral hygiene status, and salivary properties (including viscosity, hydration, flow rate, pH, buffering capacity, calcium, phosphorus, IgA, and Streptococcus mutans count) in children aged 3-12 years with CHD at risk of IE versus healthy controls, while assessing parental KAP regarding oral health and IE prevention. Specific objectives included (1) assessing clinical indices (DMFT/deft and OHI-S), (2) analyzing salivary parameters using standardized kits and biochemical assays, (3) quantifying Streptococcus mutans via microbial culture, and (4) evaluating parental KAP through a validated questionnaire to identify differences and recommend educational strategies.

2. Methodology

2.1. Study design

This cross-sectional comparative study was conducted in the Department of Pediatric and Preventive Dentistry at Sardar Patel Post Graduate Institute of Dental and Medical Sciences, Lucknow, India, in collaboration with the Department of Microbiology at the same institute, the Department of Cardiology at Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, and the A pilot study was initially performed in the same departments to refine the study design and address potential constraints. The main study was divided into two phases: Phase I focused on interviewing parents/caregivers to assess KAP, and Phase II involved clinical examination and salivary analysis of children.

2.2. Participant selection

Participants were recruited into two groups: Group A (Cases): children aged 3–12 years with a confirmed diagnosis of CHD classified as at risk for Infective Endocarditis (IE) according to the 2017 American Heart Association (AHA) guidelines (e.g., unrepaired cyanotic CHD, prosthetic valves, previous IE). Group B (Controls): age- (±6 months) and sex-matched healthy children with no systemic illness, recruited from pediatric dental clinics. To minimize socioeconomic confounding, an attempt was made to match groups based on parental education level. Exclusion criteria for both groups included antibiotic use within the past month, other systemic diseases affecting oral health (e.g., diabetes, immunodeficiencies), and uncooperative behavior.

2.3. Ethical approval

The study protocol was approved by the Institutional Ethical Committee (approval number: SPGDH/ETH/2022/34). Participation was voluntary and informed consent was obtained from all parents/caregivers prior to enrolment. Anonymity was maintained by not collecting personal identifiers, and electronic medical records were reviewed solely to confirm CHD diagnoses according to the American Heart Association (AHA) criteria for infective endocarditis (IE) risk (2017 guidelines).6 Parents/caregivers were provided with a detailed explanation of the study procedures, and investigators were available for clarification during data collection.

2.4. Sample size calculation

The sample size was calculated to compare mean dmft scores between children with congenital heart disease (CHD) and healthy controls. Based on a previously reported effect size of 0.46 for dmft, with 80% power and a 5% alpha error (two-tailed), the required sample was 60 participants per group. Considering a 10% potential dropout rate, the final sample size was increased to 65 children in each group.

2.5. Questionnaire development and validation for parental KAP assessment (Phase I)

A self-constructed, validated questionnaire was used to assess parental KAP regarding oral health and IE risks. The questionnaire was developed based on information from the World Health Organization (WHO) collaborating centre for community oral health programs. The questionnaire was validated for content by a panel of five experts (pediatric cardiologists, pediatric dentists, epidemiologists) and for face validity via pilot testing on 20 parents (not included in the main study). Internal consistency was acceptable (Cronbach's alpha = 0.74). The survey comprised 16 multiple-choice questions: two on demographics (child's age and sex), eight on knowledge (such as awareness of plaque, gingivitis prevention, and oral-cardiac health links), four on attitude (such as importance of dental visits and sweets' impact on teeth), and two on perception (such as interest in oral health education). Data were collected via face-to-face interviews conducted by two investigators to ensure comprehension and accuracy.

2.6. Clinical assessment (Phase II: Part I)

Children from both groups underwent intraoral examination under natural light using sterile mouth mirrors, explorers, and Community Periodontal Index (CPI) probes, as recommended by the WHO. Dental caries status was recorded using the Decayed, Missing, Filled Teeth (DMFT) index for permanent dentition and the decayed, extracted, and filled teeth (deft) index for primary dentition. Oral hygiene status was evaluated using the Simplified Oral Hygiene Index (OHI-S), which assesses debris and calculus on selected tooth surfaces.10 All examinations were performed by calibrated investigators to minimize bias and intra-examiner reliability was assessed using kappa statistics (kappa >0.8).

2.7. Salivary assessment (Phase II: Part II)

Unstimulated saliva samples were collected after instructing participants to abstain from eating, drinking, brushing, or chewing gum for at least 1 h prior. Salivary properties were evaluated using a GC Saliva-Check BUFFER kit (GC Corporation, Tokyo, Japan). Hydration was assessed by observing minor salivary gland secretion on the everted lower lip after blotting with gauze. Low hydration was noted if droplets formed after >1 min. Viscosity was visually inspected from expectorated saliva: normal if clear and watery, and increased if frothy, sticky, or stringy. Resting pH was measured by immersing test strips in pooled saliva for 10 s and comparing colors to a scale (highly acidic: 5.0–5.8; moderately acidic: 6.0–6.6; healthy: 6.8–7.8). Stimulated salivary flow was determined by chewing unflavored paraffin wax for 5 min, with collection in a graduated cup (very low: <3.5 mL; low: 3.5–5.0. mL; normal: >5.0 mL). Buffering capacity was tested by applying stimulated saliva to the test pads and scoring color changes after 2 min (very low: 0–5 points; low: 6–9 points; normal: 10–12 points).

2.8. Biochemical analysis of saliva (Phase II: Part III)

Whole unstimulated saliva was collected between 10 and 11 a.m. in sterile vials using the method described by Dawes to account for circadian variations. Samples were centrifuged at 282 × g for 5 min at 25°C for calcium and phosphorus analysis; supernatants were aliquoted and stored at −70°C before transport to the biochemistry department. Calcium and phosphorus levels were quantified using standard biochemical assays. For secretory IgA (sIgA), samples were centrifuged at 10,000 × g for 15 min at 4°C, and supernatants were analyzed using enzyme-linked immunosorbent assay (ELISA) (IgA Secretory ELISA, Invitrogen, Catalog #88-50600-22), according to the manufacturer's protocol at the collaborating biochemistry laboratory.

2.9. Microbiological analysis for Streptococcus mutans count (Phase II: Part IV)

For the quantification of Streptococcus mutans, saliva samples were processed within 1 h of collection. Serial ten-fold dilutions were prepared in sterile phosphate-buffered saline and plated in triplicate on Mitis Salivarius Bacitracin (MSB) agar selective plates. Plates were incubated microaerophilically (85% N2, 10% CO2, 5% H2) at 37°C for 48 h. Colonies exhibiting characteristic morphology (small, opaque, adherent, frosted-glass appearance) were counted as colony-forming units per milliliter of saliva (CFU/mL). The lower limit of detection for this method was 1.0 × 102 CFU/mL. Counts were log10-transformed for statistical analysis.

2.10. Statistical analysis

Data were analyzed using IBM SPSS Statistics for Windows, Version 26 (IBM Corp., Armonk, NY, USA). Descriptive statistics were used to summarize the data. Normal distribution was assessed using the Shapiro-Wilk test. Independent t-tests were used to compare continuous variables (OHI-S, DMFT, and saliva parameters) between groups. Chi-square tests were applied to the categorical parental KAP outcomes. Pearson's correlation was used to analyze the relationship between salivary factors and caries scores. Multiple linear regression models were used to predict oral health outcomes (DMFT and OHI-S) from independent variables (CHD status, salivary parameters, and parental KAP scores), controlling for confounders, such as age, sex, and sugar intake frequency. All tests were two-tailed, with a significance level of p < 0.05.

3. Results

A total of 130 children aged 3–12 years were included in the study, comprising 65 children with CHD and 65 age- and sex-matched healthy controls. Complete clinical and questionnaire data were available for all the participants. Salivary analysis was completed for 62 children in each group because of insufficient sample volume in a few cases.

3.1. Baseline characteristics

The CHD and control groups were comparable with respect to age and sex distribution, with no statistically significant differences (p > 0.05). Children in the CHD group had a significantly higher mean daily sugar intake frequency and poorer dental attendance patterns than those in the control group (p < 0.05). All children in the CHD group were on cardiac medications, and cyanotic CHD constituted the majority of the cases (Table 1).

Table 1.

Baseline characteristics of study participants.

Demographics Characteristics CHD Group (n = 65) Control Group (n = 65) p-value
Age (years), mean ± SD 7.4 ± 2.8 7.2 ± 2.6 0.68
Sex, n (%)
Male 36 (55.3) 34 (52.3) 0.82
Female 29 (44.7) 31 (47.7)
CHD classification
Cyanotic CHD, n (%) 40 (61.5) 0 (0) 0.001*
Acyanotic CHD, n (%) 25 (38.5) 0 (0) 0.001*
On cardiac medication, n (%) 65 (100) 0 (0) 0.001*
Dietary habits
Sugar intake frequency (times/day), mean ± SD 3.8 ± 1.5 2.2 ± 1.0 0.001*
Last dental visit, n (%)
Within 6 months 13 (20.0) 26 (40.3) 0.01*
6-12 months 16 (24.6) 21 (32.3)
>12 months 19 (29.2) 13 (19.4)
Never 17 (26.2) 5 (8.1)

*Statistically significant at p < 0.05.

3.2. Oral health status and salivary parameters

Children with CHD demonstrated significantly higher caries experience in the primary dentition (dmft) and poorer oral hygiene status (OHI-S) than healthy controls (p < 0.001). The CHD group exhibited a significantly lower unstimulated salivary flow rate, pH, and buffering capacity, along with significantly higher salivary viscosity, osmolality, and Streptococcus mutans counts (p < 0.001). No statistically significant difference was observed in salivary calcium levels between the two groups. These findings demonstrate that CHD is associated with the pathological triad of severe caries, poor hygiene, and dysfunctional saliva. Hyposalivation, reduced buffering, and elevated cariogenic bacteria create a perfect environment for rapid decay (Table 2).

Table 2.

Comparison of oral health status and salivary parameters between the groups.

Parameter CHD Group (n = 62) Control Group (n = 62) Mean Difference (95% CI) p-value
Oral Health Indices
DMFT score, mean ± SD 5.8 ± 3.5 2.3 ± 2.1 3.5 (2.6, 4.4) 0.001*
OHI-S score, mean ± SD 2.8 ± 0.9 1.4 ± 0.6 1.4 (1.1, 1.7) 0.001*
Salivary flow and properties
Unstimulated flow rate (mL/min), mean ± SD 0.18 ± 0.08 0.32 ± 0.10 −0.14 (−0.17, −0.11) 0.001*
pH, mean ± SD 6.8 ± 0.4 7.2 ± 0.3 −0.4 (−0.5, −0.3) 0.001*
Buffering capacity (ΔpH), mean ± SD 1.2 ± 0.5 2.1 ± 0.6 −0.9 (−1.1, −0.7) 0.001*
Viscosity (cP), mean ± SD 3.8 ± 1.2 2.1 ± 0.8 1.7 (1.3, 2.1) 0.001*
Hydration (osmolality, mOsm/kg), mean ± SD 285 ± 45 245 ± 32 40 (27, 53) 0.001*
Salivary biochemical parameters
Calcium (mg/dL), mean ± SD 6.2 ± 1.8 5.8 ± 1.5 0.4 (−0.2, 1.0) 0.17
Phosphorus (mg/dL), mean ± SD 14.5 ± 3.2 15.8 ± 2.9 −1.3 (−2.4, −0.2) 0.02*
Secretory IgA (μg/mL), mean ± SD 185 ± 65 210 ± 58 −25 (−47, −3) 0.03*
Microbiological parameter
S. mutans count (log10 CFU/mL), mean ± SD 4.8 ± 0.9 3.2 ± 0.7 1.6 (1.3, 1.9) 0.001*

*Statistically significant at p < 0.05.

3.3. Parental knowledge, attitude, and practice (KAP)

Parents of children with CHD had significantly lower knowledge, attitude, and practice scores than those of healthy children (p < 0.001). Supervised tooth brushing, regular dental visits, and dietary sugar restriction practices were significantly less frequently reported by parents in the CHD group. This profound KAP deficit among CHD parents likely represents a major modifiable contributor to their children's poor oral health, suggesting that the complexity of cardiac care may overshadow oral health priorities. Therefore, targeted educational interventions aimed at parents with CHD are urgently needed as part of an integrated care model to improve preventive practices and break the cycle of dental disease in this vulnerable population (Table 3).

Table 3.

Parental knowledge, attitude, and practice (KAP) scores.

KAP Domain Control Group Parents (n = 65) CHD Group Parents (n = 65) Mean Difference (95% CI) p-value
Knowledge (Max score-15)
Total score, mean ± SD 11.8 ± 2.1 8.2 ± 2.5 −3.6 (−4.4, −2.8) 0.001*
CHD-specific oral care knowledge, n (%) correct 47 (72.6) 16 (24.2) −48.4% 0.001*
Caries etiology knowledge, n (%) correct 52 (80.0) 29 (44.6) −38.7% 0.001*
Attitude (Max score-50)
Total score, mean ± SD 41.2 ± 5.5 32.5 ± 6.8 −8.7 (−10.8, −6.6) 0.001*
Perceived importance of oral health, mean ± SD10 8.5 ± 1.2 6.8 ± 1.8 −1.7 (−2.2, −1.2) 0.001*
Dental anxiety (reverse scored), mean ± SD10 8.8 ± 1.1 7.2 ± 1.5 −1.6 (−2.1, −1.1) 0.001*
Practice (Max score-30)
Total score, mean ± SD 24.8 ± 3.8 18.5 ± 4.2 −6.3 (−7.7, −4.9) 0.001*
Supervised brushing, n (%) 48 (73.8) 22 (33.8) −40.0% 0.001*
Regular dental visits, n (%) 42 (64.6) 18 (27.6) −37.0% 0.001*
Sugar restriction practice, n (%) 38 (58.4) 15 (23.1) −35.3% 0.001*

*Statistically significant at p < 0.05.

3.4. Correlation and regression analysis

Pearson's correlation analysis (Table 4) demonstrated statistically significant associations between the oral health indices and salivary parameters. The DMFT score showed a strong positive correlation with S. mutans count and salivary viscosity and a moderate negative correlation with salivary flow rate, pH, and buffering capacity. Similarly, OHI-S scores were positively correlated with S. mutans count and viscosity and negatively correlated with salivary flow rate and pH. Secretory IgA showed weak but significant negative correlations with DMFT and salivary viscosity. No statistically significant correlations were observed between the DMFT or OHI-S scores and salivary calcium levels.

Table 4.

Pearson correlation between salivary parameters and oral health indices (n = 130).

Variable DMFT OHI-S Flow Rate pH Buffering Viscosity Secretory IgA (μg/mL) S. mutans
DMFT 1.00
OHI-S 0.68** 1.00
Salivary flow rate (mL/min) −0.45** −0.38** 1.00
Salivary pH −0.42** −0.35** 0.52** 1.00
Buffering capacity (ΔpH) −0.38** −0.32** 0.48** 0.65** 1.00
Salivary viscosity (cP) 0.51** 0.44** −0.56** −0.48** −0.42** 1.00
Secretory IgA (μg/mL) −0.22* −0.18 0.25* 0.30** 0.28** −0.20* 1.00
Streptococcus mutans (log10 CFU/mL) 0.62** 0.55** −0.51** −0.45** −0.40** 0.58** −0.25* 1.00
Hydration (osmolality, mOsm/kg) 0.48** 0.41** −0.53** −0.46** −0.39** 0.62** −0.22* 0.55**
Salivary calcium (mg/dL) 0.08 0.05 −0.12 −0.10 −0.08 0.15 0.02 0.12
Salivary phosphorus (mg/dL) −0.15 −0.12 0.18 0.22* 0.20* −0.16 0.10 −0.18

Pearson correlation coefficients shown. *p < 0.05, **p < 0.01.

Hydration, calcium, and phosphorus included in analysis but limited by table width.

Multiple linear regression analysis (Table 5) showed that CHD status remained a significant independent predictor of both DMFT and OHI-S scores after adjusting for confounders (p < 0.001). Lower salivary flow rate, lower salivary pH, higher salivary viscosity, and higher S. mutans counts were significantly associated with increased DMFT and OHI-S scores (P < 0.05). Higher sugar intake frequency was positively associated, whereas higher parental knowledge and practice scores were negatively associated with both outcomes (p < 0.05).

Table 5.

Multiple linear regression analysis for predictors of oral health outcomes.

Predictor Model 1: DMFT Score
Model 2: OHI-S Score
β (95% CI) p-value β (95% CI) p-value
Constant 8.25 (6.12, 10.38) 0.001* 3.85 (2.45, 5.25) 0.001*
Group Status
CHD (ref: Control) 1.85 (0.95, 2.75) 0.001* 0.65 (0.35, 0.95) 0.001*
Salivary Parameters
Flow rate (per 0.1 mL/min increase) −0.45 (−0.75, −0.15) 0.004* −0.18 (−0.28, −0.08) 0.001*
pH (per 0.5-unit increase) −0.65 (−1.15, −0.15) 0.01* −0.25 (−0.45, −0.05) 0.02*
Viscosity (per 1 cP increase) 0.55 (0.25, 0.85) 0.001* 0.22 (0.12, 0.32) 0.001*
S. mutans (per 1 log10 CFU/mL) 0.95 (0.55, 1.35) 0.001* 0.38 (0.18, 0.58) 0.001*
Parental Factors
Knowledge score (per point) −0.25 (−0.45, −0.05) 0.02* −0.10 (−0.18, −0.02) 0.02*
Practice score (per point) −0.30 (−0.50, −0.10) 0.004* −0.12 (−0.20, −0.04) 0.004*
Covariates
Age (per year) 0.15 (0.05, 0.25) 0.004* 0.05 (0.01, 0.09) 0.02*
Sugar intake (per episode/day) 0.35 (0.15, 0.55) 0.001* 0.12 (0.04, 0.20) 0.004*
Last dental visit (>12 months vs. ≤12) 0.75 (0.25, 1.25) 0.004* 0.25 (0.05, 0.45) 0.02*

β = unstandardized regression coefficient; *p < 0.05.

4. Discussion

The present study highlights pronounced differences in oral health outcomes, salivary protective mechanisms, and parental KAP between children with CHD who are at risk of infective endocarditis (IE) and healthy controls. These disparities can be attributed to the complex interplay between medical management, dietary factors, medication effects, and behavioral priorities in the CHD population.

Children with CHD frequently experience poorer oral hygiene and elevated caries prevalence due to prolonged exposure to cariogenic medications, which often contain fermentable carbohydrates and acidic excipients that lower intraoral pH and promote microbial adhesion. Frequent sugar intake, which is common in this group to improve compliance with cardiac drugs, further exacerbates demineralization.11 Additionally, cyanotic forms of CHD may contribute to developmental enamel defects through chronic hypoxia, increasing susceptibility to caries initiation and progression. Salivary hypofunction, manifested as reduced flow rates, lowered pH, diminished buffering capacity, increased viscosity, and higher osmolality, impairs natural remineralization, acid neutralization, and antimicrobial clearance. Similar findings have been reported previously.4,11,12

Alterations in salivary parameters, such as pH, osmolarity, and buffering capacity, favor the proliferation of acidogenic bacteria, particularly Streptococcus mutans, leading to higher microbial counts and biofilm formation. Lower levels of protective biochemical components, such as phosphorus and secretory IgA, contribute to this vulnerability by reducing remineralization potential and mucosal immunity.3,13 In contrast, Franco et al.14 reported no significant difference in salivary IgA levels and S. mutans counts between the control group and children with CHD; however, they noted a high caries index and the presence of a greater amount of untreated disease in children with CHD.

Parental factors play a critical role in perpetuating these problems. In families managing CHD, cardiac concerns often overshadow routine oral care, resulting in less emphasis on preventive practices, such as supervised brushing, sugar restriction, and timely dental visits. Limited awareness of the oral-systemic link, including how poor oral hygiene contributes to transient bacteremia and IE risk, leads to inadequate knowledge of specific preventive measures and lower motivation for consistent oral health behaviors.

These findings align with those of previous research, particularly in highlighting the elevated caries risk and compromised salivary defences in children with CHD. Systematic reviews have consistently indicated a higher caries prevalence in this population compared to healthy peers, often linked to medication-related factors and enamel anomalies.4 Studies in diverse settings have reported similar patterns of reduced salivary flow, pH, and buffering capacity, attributing these to xerostomia induced by cardiac medications and overall physiological stress.3 Elevated S. mutans has been documented in multiple cohorts, reinforcing its role in caries progression in altered salivary environments.6,13 In the Indian context, investigations have emphasized poor oral hygiene practices, high plaque accumulation, and medication-driven risks, underscoring regional challenges such as socioeconomic barriers and prioritization of cardiac over dental care.4,15 Hypoxia in cyanotic CHD is another potent factor contributing to the increased incidence of dental caries in children with CHD.

Parental KAP deficits echo both global and local patterns. Numerous studies have demonstrated fair to limited knowledge among parents of children with CHD regarding the connection between oral health and IE prevention, with unsatisfactory attitudes toward routine dental care and preventive behaviors.16,17. In developing countries, including India, parents often exhibit gaps in their understanding of antibiotic prophylaxis, the importance of regular check-ups, and daily hygiene routines, leading to irregular dental attendance and suboptimal practices.18 Recent interventions, such as mobile application-based education, have shown promise in improving KAP scores and reducing plaque indices, suggesting that targeted awareness programs could effectively address these shortcomings.19

Clinically, these results underscore the need for integrated, multidisciplinary care. Routine oral health screening in pediatric cardiology settings combined with early parental education on IE risk from oral sources is essential. Emphasis on fluoride applications, salivary stimulants, and dietary counselling could mitigate salivary deficits; however, reinforcing the AHA guidelines for prophylaxis during invasive procedures remains vital. Community-level initiatives, including workshops and digital tools, can enhance parental engagement and reduce long-term IE morbidity in resource-constrained Indian settings.

The limitations of the study include its cross-sectional design, which precludes establishing causality and reliance on convenience sampling from a single tertiary centre, potentially limiting generalizability across diverse Indian populations. Self-reported KAP data may introduce recall or social desirability bias, and unmeasured confounders, such as detailed socioeconomic status or specific medication types, warrant consideration in future work. Longitudinal multicentre studies incorporating targeted interventions are recommended to build on these insights and evaluate sustainable improvements.

Another limitation of the present study is the heterogeneity within the CHD group, which included children with varying cardiac defects (cyanotic and acyanotic), disease severities, and surgical statuses. These clinical differences may independently influence oral health and salivary characteristics, potentially introducing variability in the observed outcomes. Future stratified multicentric studies are recommended to better evaluate these subgroup-specific effects.

5. Conclusion

This study demonstrated that children with CHD at risk of IE exhibited significantly poorer oral health, compromised salivary protective properties, and elevated Streptococcus mutans counts compared to healthy controls. These findings are largely attributable to medication-related cariogenic effects, salivary hypofunction, and notably deficient parental knowledge, attitudes, and preventive practices regarding oral-systemic links. These results highlight the urgent need for integrated pediatric cardiology and dental care in India. Routine oral screening should be prioritized with targeted parental education programs and early preventive interventions to reduce the caries burden and mitigate the risk of IE in this vulnerable population.

Ethical statement

The study was conducted in accordance with the ethical principles of the Declaration of Helsinki. Ethical approval for the study was obtained from the Institutional Ethical Committee, Sardar Patel Post Graduate Institute of Dental & Medical Sciences (SPPGIDMS), Lucknow, vide Ref. No. FR/01/IEC/SPPGIDMS/2026, dated 20 January 2026. Written informed consent was obtained from the parents/legally authorized representatives of all participating children prior to their inclusion in the study. The confidentiality and privacy of the participants were maintained throughout the study.

Source of funding

The authors received no financial support or funding from any public, commercial, or not-for-profit organization for the conduct of this study.

Ethical approval and consent to participate

All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. Ethical approval was obtained from the Institutional Review Board/Ethics Committee (Approval No.: __FR/01/IEC/SPPGIDMS/2026____).

Informed consent was obtained from the parents/guardians of all participating children prior to inclusion in the study.

Declaration of competing interest

The authors declare that there are no conflicts of interest associated with this study.

Acknowledgement

The authors would like to express their sincere gratitude to the Institutional Ethical Committee, Sardar Patel Post Graduate Institute of Dental & Medical Sciences, Lucknow, for reviewing and granting ethical approval for this study. The authors are also grateful to the participating children and their parents/guardians for their valuable cooperation and participation. We acknowledge the support and cooperation extended by the faculty, staff, and concerned departments during the conduct of the study.

References

  • 1.van der Linde D., Konings E.E., Slager M.A., et al. Birth prevalence of congenital heart disease worldwide: a systematic review and meta-analysis. J Am Coll Cardiol. 2011;58:2241–2247. doi: 10.1016/j.jacc.2011.08.025. [DOI] [PubMed] [Google Scholar]
  • 2.Saxena A. Congenital heart disease in India: a status report. Indian Pediatr. 2018;55:1075–1082. https://pubmed.ncbi.nlm.nih.gov/30745481/ [PubMed] [Google Scholar]
  • 3.Koruyucu M., Batu S., Bayram M., Uslu E., Guven Y., Seymen F. Saliva profiles in children with congenital heart disease. Eur Oral Res. 2020;54:48–54. doi: 10.26650/eor.20200087. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Karikoski E., Sarkola T., Blomqvist M. Dental caries prevalence in children with congenital heart disease - a systematic review. Acta Odontol Scand. 2021;79:232–240. doi: 10.1080/00016357.2020.1849792. [DOI] [PubMed] [Google Scholar]
  • 5.Rushani D., Kaufman J.S., Ionescu-Ittu R., et al. Infective endocarditis in children with congenital heart disease: cumulative incidence and predictors. Circulation. 2013;128:1412–1419. doi: 10.1161/CIRCULATIONAHA.113.001827. [DOI] [PubMed] [Google Scholar]
  • 6.Desimone D.C., Tleyjeh I.M., Correa de Sa D.D., et al. Incidence of infective endocarditis caused by viridans group streptococci before and after publication of the 2007 American Heart Association's endocarditis prevention guidelines. Circulation. 2012;126:60–64. doi: 10.1161/CIRCULATIONAHA.112.095281. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Lockhart P.B., Brennan M.T., Thornhill M., et al. Poor oral hygiene as a risk factor for infective endocarditis-related bacteremia. J Am Dent Assoc. 2009;140:1238–1244. doi: 10.14219/jada.archive.2009.0046. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Hegde A.M., Kavita R., Sushma K.S., Suchetha S. Salivary sialic acid levels and dental health in children with congenital heart disease. J Clin Pediatr Dent. 2012;36:293–296. doi: 10.17796/jcpd.36.3.t585vt7v125630q4. [DOI] [PubMed] [Google Scholar]
  • 9.Schulz-Weidner N., Logeswaran T., Schlenz M.A., Krämer N., Bulski J.C. Parental awareness of oral health and nutritional behavior in children with congenital heart diseases compared to healthy children. Int J Environ Res Publ Health. 2020;17:7057. doi: 10.3390/ijerph17197057. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Greene J.C., Vermillion J.R. The simplified oral hygiene index. J Am Dent Assoc. 1964;68:7–13. doi: 10.14219/jada.archive.1964.0034. [DOI] [PubMed] [Google Scholar]
  • 11.Stecksén-Blicks C., Rydberg A., Nyman L., Asplund S., Svanberg C. Dental caries experience in children with congenital heart disease: a case-control study. Int J Paediatr Dent. 2004;14:94–100. doi: 10.1111/j.1365-263x.2004.00531.x. [DOI] [PubMed] [Google Scholar]
  • 12.Koerdt S., Hartz J., Hollatz S., et al. Prevalence of dental caries in children with congenital heart disease. BMC Pediatr. 2022 12;22:711. doi: 10.1186/s12887-022-03769-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Pollard M.A., Curzon M.E. Dental health and salivary Streptococcus mutans levels in a group of children with heart defects. Int J Paediatr Dent. 1992;2:81–85. doi: 10.1111/j.1365-263x.1992.tb00014.x. [DOI] [PubMed] [Google Scholar]
  • 14.Franco E., Saunders C.P., Roberts G.J., Suwanprasit A. Dental disease, caries related microflora and salivary IgA of children with severe congenital cardiac disease: an epidemiological and oral microbial survey. Pediatr Dent. 1996;18:228–235. https://pubmed.ncbi.nlm.nih.gov/8784915/ [PubMed] [Google Scholar]
  • 15.Hazarika S.J., Jnaneswar A., Jha K. A comparative assessment of dental caries experience in relation to nutritional status among 6-12-year-old school-going children and those with congenital heart disease in Bhubaneswar City. Int J Clin Pediatr Dent. 2024;17:1–6. doi: 10.5005/jp-journals-10005-2595. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Rai K., Supriya S., Hegde A.M. Oral health status of children with congenital heart disease and the awareness, attitude and knowledge of their parents. J Clin Pediatr Dent. 2009;33:315–318. doi: 10.17796/jcpd.33.4.2j108w0225241867. [DOI] [PubMed] [Google Scholar]
  • 17.AlSuliman F.S., Alajlan S.A., Algonaid O.A., Almashham L.Y., Alawaji R.H. Knowledge, attitude, and perception of oral health among parents of children at risk of infective endocarditis: a cross-sectional study. Cureus. 2023;15 doi: 10.7759/cureus.44855. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Suvarna R., Rai K., Hegde A.M. Knowledge and oral health attitudes among parents of children with congenital heart disease. Int J Clin Pediatr Dent. 2011;4:25–28. doi: 10.5005/jp-journals-10005-1076. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 19.Ajay K., Azevedo L.B., Haste A., et al. App-based oral health promotion interventions on modifiable risk factors associated with early childhood caries: a systematic review. Front Oral Health. 2023;10(4) doi: 10.3389/froh.2023.1125070. [DOI] [PMC free article] [PubMed] [Google Scholar]

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