Oral microflora and dietary intake in infants with congenital heart disease: a case control study.
Congenital heart disease (CHD) is one of the most common congenital anomalies in children. The incidence of severe to moderately severe CHD is 6 per 1,000 live births [Hoffman and Kaplan, 2002; Hoffman et al., 2004]. Progress in medical and surgical treatment has resulted in increased survival, and today a majority of the children with CHD reach adulthood. Although the medical care for children with CHD has improved, this group of patients still have special needs. In the first year of life, malnutrition is common, and adequate dietary intake is a major challenge. Studies have shown complex nutritional difficulties in early infancy [Ackerman et al., 1998; Vieira et al., 2007; Jadcherla et al., 2009; Nydegger et al., 2009]. Regular vomiting, sometimes induced by drug-related nausea or reduced gastric capacity, is also a well-recognised problem in infants with CHD. To compensate for the increased metabolic requirements and limited caloric intake, infants with CHD have to eat more frequently than healthy children, and their food has to be enriched with nutrients and energy. The beneficial effects of the superior nutritional intake on the health of infants with CHD are clear. However, the dietary modifications may have a negative impact on the oral health of these children and increase the risk of dental caries [Selwitz et al., 2007]; as a consequence, infective endocarditis may result [Balmer and Bu'Lock, 2003; Moursi et al., 2010].
Long-term medication is another factor that may affect oral health [Moore and Guggenheimer, 2008; Maupome et al., 2010]. Diuretics increase the excretion of water from the circulatory system and are routinely used to treat heart failure in these patients. Reduced saliva and altered salivary flow are known side effects of diuretics [Scully and Felix, 2005]. Disturbed mineralisation in teeth has also been reported [Hakala and Haavikko,1974]. Sucrose is still used as a sweetener in some drugs, to enhance flavour [Bigeard, 2000; Moursi et al., 2010]. Despite good dental care and intensive prevention, poorer dental health has been seen in children with CHD than in healthy children [Stecksen-Blicks et al., 2004].
The aim of this study was to examine oral colonisation of some bacteria associated with caries development during infancy in children with severe CHD, and to investigate its association with dietary intake early in life, particularly with carbohydrate consumption and meal patterns. The null hypothesis was that there are no differences between children with CHD and healthy controls.
Subjects: Patients and controls Seventeen infants between 6-12 months of age, with severe CHD were recruited from the Paediatric Cardiology Outpatient Clinic at the University Hospital in Umea, Sweden, for this prospective case-control study. 4 children were excluded from the study because of the diagnosis of an associated syndrome and medical co-morbidities, and 2 families declined participation. Thus, 11 infants (aged 6 months) with severe CHD were included (Table 1). To match the feeding patterns of the CHD children, 31 formula-fed healthy controls of the same age and gender were recruited from Child Health Clinics in the area. Infants that were exclusively breastfed for more than a few weeks were excluded. 6 of the families declined participation, and 3 infants were excluded; one on account of being prematurely born, and two that were still being breastfed. Thus, 22 infants were enrolled in the study as controls. All children were living in the counties of Vasterbotten and Vasternorrland in northern Sweden. Written informed consent was obtained before inclusion. The study was approved by the Regional Ethical Review Board, Umea University.
Diagnosis, medications, and use of antibiotics Data on diagnosis, medications, and use of antibiotics for the CHD group were collected from the medical records at the Paediatric Clinics of the University Hospital in Umea and the Hospital in Skelleftea. For the controls, data was obtained from the records at the Paediatric Clinic in Umea and the Child Health Clinics in Umea and Ornskoldsvik communities. At baseline, the parents were questioned about their educational level, as well as the health status and body weight of their children. The educational levels were categorised into 9-year compulsory school, upper secondary school education, and university studies.
Bacterial colonisation At 6, 9, and 12 months of age, an oral sampling was performed as described by Twetman and Grindefjord . In brief, a wooden, saline-wetted cotton bud was gently streaked along the buccal mucosa in the anterior part of the mandible and maxilla of each child; in cases with tooth eruption, the streaking was done along the mandibular and maxillary incisors. The cotton bud was transferred to a transport medium with 1 ml M-dil. The samples were serially diluted in a NaCl-containing potassium phosphate buffer to obtain 0-, 40-, 800-, and 8,000-fold dilutions. Next, 50-ul aliquots were plated onto 2 different selective media. MS were cultivated on selective (MSB) agar (Difco Mitis Salivarius Agar, Becton, Dickinson and Company, USA) and Lactobacilli (LBC) on Man, Rogosa, Sharpe (MRS) agar (Merck, Germany). Next, 50-[micro]l aliquots of the 800-fold and 100 [micro]l of the 8,000-fold diluted suspensions were transferred to blood agar oral (BAO) plates for an estimation of the total viable counts (TVC). All plates were incubated aerobically at 37[degrees]C in 5% C[O.sub.2] for 48 h and then examined under a light microscope to verify the presence of colony forming units (CFU).
Dietary registration and body weight In concurrence with the oral sampling for determining the colonisation of bacteria at 6, 9, and 12 month of age, parents were asked to complete a 3-day food diary, including the time, type, and quantity of each food item consumed by the infant. Quantities were recorded in household measures. The total energy intake, amount of proteins, fats, carbohydrates, sucrose, and meal frequency was calculated for each infant by using Dietist XP, version 3.1 (Kost och Naringsdata, Stockholm 2010), which includes the Swedish National Food Database from the National Food Administration and food tables from food companies. The database was supplemented with food recipes and baby food not originally included in the Dietist XP, as per the information obtained from the parents and food manufacturers. Weight tables from National Food Administration were used for estimating the weight of the food or formula [Swedish National Food Administration, 2000]. To calculate the meal frequency, food eaten within a 45-min time period was set as one meal. Night meals were defined as meals consumed between 11 pm and 5 am. The current body weight of the child was also recorded in the questionnaire.
The saliva samples and food diaries of three of the CHD infants that were at hospitals located in other parts of Sweden were incomplete at the 9-month time point. Two of these three infants were in a unit for the critically ill, after undergoing heart surgery, and one did not respond; thus, we could not obtain samples or food diaries. Another five parents did not return the diaries to the researchers even after several reminders, one at 6 months of age, two at 12 months of age in the control group, and two at 12 months in the CHD group. Unfortunately, one saliva sample obtained at 12 months was destroyed.
Oral examination At 12 months of age, an oral examination was performed. The number of erupted teeth, and any sign of caries was recorded. The accompanying parent was questioned about oral hygiene habits and use of fluoride toothpaste.
Statistical analysis Statistical data were processed with PASW Statistics version 18.0 (Chicago Ill, USA). Bacterial counts were log transformed prior to the statistical analysis. Chi-square test was used to test proportions. Analysis of variance, ANOVA, was used to test continuous data. A p-value of less than 0.05 was considered as statistically significant.
Characteristics of the participants There were no differences in the educational level among parents of the CHD group and those of the healthy controls (p > 0.05). In both groups, 9% of the children were delivered by caesarean section (one child in the CHD group and two children in the control group). Across all ages, body weight was significantly lower in the CHD group than in the control group (p < 0.05), (Table 2).
Medication All children in the CHD group were on diuretic medication for heart failure; 4 patients were also on salicylic acid, 4 were on potassium citrate, and 4 on spironolactone, in combination (Table 1). During the study period, the use of antibiotics was higher in infants with CHD. At 6, 9, and 12 months of age, a total of 21 antibiotic courses from birth or since the previous registration were recorded for the CHD group; the control group, on the other hand, had registered only 6 antibiotic courses (p < 0.05). 6 of the CHD patients had received antibiotic therapy before 6 months of age, whereas no child in the control group received antibiotics before that age; 2 of the CHD patients had used antibiotics continuously from birth to 12 months of age.
Dietary intake The dietary intakes at 6, 9, and 12 months of age are shown in Table 2. The total energy intake did not differ between the CHD group and the controls at any age (p > 0.05). There was a tendency for a higher energy intake in relation to bodyweight in the CHD group at all ages, but the differences were not statistically significant. Regarding the total carbohydrate intake there was a statistically significant higher intake in grams among the controls at 6 and 12 months of age (p < 0.05). The percentage intake (E%) of carbohydrates was also significantly higher among the controls at 12 months of age (p < 0.05). The sucrose intake did not differ between the CHD group and the controls (p > 0.05). There was a tendency for a higher intake of fat in the CHD group at 9 and 12 months of age, but the differences were not statistically significant (p > 0.05). The percent energy intake (E%) from fat was statistically higher in the CHD group at 9 and 12 months of age (p < 0.05) than that in the controls. The meal frequency was higher in the CHD group at 6 and 9 months of age (p < 0.05) while no differences in the frequency of night meals were evident between the two groups (p > 0.05).
Caries-associated microflora Table 3 shows the rate of MS colonisation, which was statistically significantly higher in the CHD group than in the control group at 12 months of age (p < 0.01), but not at 6 and 9 months of age. Additionally, the MS ratio of TVC was significantly higher in the CHD group at 12 months of age (p < 0.01), but not at 6 and 9 months of age (p > 0.05). At 12 months of age, 90% of the CHD group and 54% of the control group had detectable levels of MS, but this difference was not statistically significant (p = 0.056). At 6, 9, and 12 months of age, no child in the CHD group had detectable levels of LBC while, two and one children, respectively in the control group had detectable levels of LBC.
Signs of caries, oral hygiene, and use of toothpaste At 12 months of age, no child had signs of caries. In the CHD group, parents reported starting tooth brushing at 7.4 [+ or -] 3.1 months of age as compared to 8.9 [+ or -] 2.8 months for the controls (p > 0.05). The mean frequency of daily brushing was 1.3 [+ or -] 0.5 in the CHD group and 0.8 [+ or -] 0.8 in the controls (p > 0.05).
The aim of this study was to examine the proportion of some caries-associated microorganisms in infants with CHD and determine if that proportion was associated with the dietary intake, particularly carbohydrate consumption and meal frequency.
A clear strength of this study was its longitudinal design, with children being followed from 6 to 12 months of age. The number of children born with significant CHD without an associated syndromes such as Downs, Noonan, Williams, and Turner was low. To increase the power of the study, two controls were included for each infant with CHD.
Colonisation with MS is a key event in early childhood caries. At 12 months of age, CHD infants had a higher number of caries-associated MS, and they constituted a higher proportion of the total flora, indicating less microbial diversity. Thus, the null hypothesis for MS colonisation was rejected. Similar findings have been found in older children with CHD [Rosen et al., 2010]. Factors associated with early MS colonisation are not well explored, particularly in children with compromised general health. It is known that parents with MS colonisation have an impact of colonisation of their children [Douglass et al., 2008]. Data on MS levels of the parents to the present children were not collected, but it is unlikely that there were significant differences between the parents of the CHD group and the controls as they had the same educational background [Meurman et al., 2010].
It has been suggested that breastfeeding is associated with a delayed colonisation of MS [Law et al., 2007]. Human milk contains components that contribute to an infant's host defence. The predominant antibody in breast milk is secretory IgA, which is directed against microorganisms and foods that are or have been present in the mother, and they can play a role as anti-mutans IgA [Hanson et al., 2001]. Compared with the previously reported 25% [Milgrom et al., 2000], our exclusively formula-fed controls contained a higher proportion of children (59%) with detectable levels of MS at 6 months of age. As 89% had been breastfed at least up to 3 months of age, and approximately 50%, up to 6 months of age.
Mode of childbirth has also been suggested to influence early colonisation with MS. In the present groups of children, less than 10% were delivered by caesarean section. In a study using DNA hybridisation technology, MS was detected in 60% of a cohort of children at 6 months of age, where 50% were born via caesarean section, but with an unknown feeding pattern from birth [Nelun Barfod et al., 2011]. Compared to the 52% of vaginally born children, 69% of the children delivered via caesarean section were positive for MS at 6 months of age. At 3 years of age, there was a tendency for higher caries prevalence among children born via caesarean section [Barfod et al., 2011].
There are three main findings that may help explain the differences in the colonisation of MS in the CHD and control groups in the present study. Firstly, meal frequency, but not the carbohydrate intake, was higher in the CHD group at 6 and 9 months of age than in the control group. A higher meal frequency is known to be a burden on dental health, as more frequent bacterial fermentation of dietary sugars results in a decreased pH in the oral biofilm, thus favouring colonisation of acid-tolerant bacteria [Selwitz et al., 2007].
A higher meal frequency is often essential for CHD infants, as failure to thrive is a common condition, often related to the type and severity of the cardiac lesion and increased energy metabolism [Nydegger et al., 2009]. The total energy expenditure is higher in infants with CHD, and normal energy intake often does not match their needs [Ackerman et al., 1998]. Thus, to compensate for the increased metabolic requirements, infants with CHD have to eat more frequently than healthy children, and the food has to be better enriched with more energy. Several extra meals are therefore an option, in order to increase the energy intake. The timing of the required intervention, surgical or catheter-based, for the cardiac anomaly during the first year of life, may also have a large impact on nutritional status. Once the heart defect has been corrected, nutritional and growth recovery is observed [Weintraub and Menahem, 1991; Vaidyanathan et al., 2009]; the correction may also explain the normalisation of meal frequency and energy needs per kilogram body weight, as was observed in our CHD children, when they reached the age of 12 months. By the time the children reach 12 months of age, most of them would have undergone at least one corrective procedure for their heart defect. The significantly lower bodyweight of the CHD children (at 6, 9, and 12 months of age) than that of the healthy children indicates the need to compensate for the increased metabolic requirements. Fat is the most common macronutrient added to enrich foods, and provides twice the energy as compared with the other two macronutrients--proteins and carbohydrates. The higher energy intake from fat, in percentage (E%), at 9 and 12 months in the CHD group supports that fat was used for compensating the energy imbalance.
[FIGURE 1 OMITTED]
Secondly, cardiac medications, such as diuretics, have been reported to affect salivary secretion and composition [Nederfors et al., 1989]. As all participating CHD children in this study were on diuretic medication, the buffering and diluting effect of saliva may have been compromised, which may have helped to favour a shift towards acid-tolerant bacteria [Selwitz et al., 2007].
[FIGURE 2 OMITTED]
The third finding, that may explain the differences in oral microflora, was the higher frequency of antibiotic use among the CHD infants as compared with the controls. CHD patients are at high risk for complications following heart failure. Some of the more complicated congenital heart diseases have accompanying asplenia, which is associated with frequent infections. Infectious endocarditis may be a rare but fatal condition in this group of patients. Therefore, antibiotic therapy in this group is often more liberal, as compared to that in healthy children, and prophylactic antibiotic use to avoid adverse outcomes from potential infections is also more frequent. The use of antibiotics in young children has been shown to be associated with a higher prevalence of MS [Dasanayake et al., 1995], possibly because of the confounding effect of sucrose found in some medications on MS colonisation.
The early high oral colonisation of MS in children with CHD indicated that this group may be at a higher risk for caries. The children with CHD had higher colonisation of MS at 12 months of age, and MS constituted a higher proportion of the total cultivatable oral microflora. A higher meal frequency and use of diuretics and antibiotics may have influenced MS colonisation.
The authors are most grateful to all the participating children and their parents. Inger Sjostrom and Elisabeth Granstrom are acknowledged for skilful laboratory assistance.
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L. Hansson *, A. Rydberg *, C. Stecksen-Blicks **
* Department of Clinical Sciences, ** Department of Odontology, Paediatric Dentistry, Umea University, Sweden
Postal address: Dr C. Stecksen-Blicks, Pediatric Dentistry, Department of Odontology, Faculty of Medicine, Umea University, S 901 85 Umea, Sweden.
Table 1. Patient characteristics. Case Diagnosis Cardiac Medication 1 PA + IVS furosemide, salicylic acid 2 CoA + VSD furosemide, potassium citrate 3 PA + AV def + TAPVR furosemide, salicylic acid, potassium citrate, spironolactone, warfarin 4 PA + VSD furosemide, salicylic acid 5 VSD (multiple) + ASD furosemide 6 PA + IVS furosemide, salicylic acid, spironolactone 7 AS + DCMP furosemide, digoxin, spironolactone 8 DILV + TGA + VSD furosemide 9 VSD (large) furosemide, potassium citrate, spironolactone 10 VSD (large) furosemide, potassium citrate, spironolactone 11 Ebstein anomaly furosemide, propranolol Diagnosis and cardiac medication in the patient group. (PA = pulmonary atresia; IVS = intact ventricular septum; VSD = ventricular septal defect; CoA = coarctation of the aorta; AV def = atrioventricular defect; TAPPV = total anomalous pulmonary venous return; AS = aortic valve stenosis; DCMP = dilated cardiomyopathy; DILV = double inlet left ventricle; TGA = transposition of the great arteries) Table 2. Dietary intake, meal frequency, and body weight at 6, 9, and 12 months of age in a study of children with CHD. CHD 6 mo n=11 9 mo n=8 12 mo n=9 mean [+ or -]SD mean [+ or -]SD mean [+ or -]SD KJ 2573.0 3711.3 3582.9 [+ or -] 1015.7 [+ or -] 764.4 [+ or -] 899 Kcal 617.6 886.7 856.0 [+ or -] 246.2 [+ or -] 177.4 [+ or -] 214.6 Proteins (g) 15.6 26. 7 28.0 [+ or -] 6.9 [+ or -] 5.0 [+ or -] 11.2 Energy % of 9.8 11.8 13.2 proteins [+ or -] 1.3 [+ or -] 1.4 [+ or -] 3.2 Fats (g) 28.9 39.7 38.1 [+ or -] 14.6 [+ or -] 10.3 [+ or -] 9.1 Energy % 40.1 40.0 39.8 of fats [+ or -] 7.7 [+ or -] 6.2* [+ or -] 4.7 ** Carbohydrates 73.0 103.4 98.5 (g) [+ or -] 25.6 [+ or -] 21.6 [+ or -] 26.0 Energy % of 49.2 47.1 46.2 carbohydrates [+ or -] 7.5 [+ or -] 5.5 [+ or -] 3.2 Sucrose (g) 1.8 3.9 4.9 [+ or -] 2.1 [+ or -] 5.5 [+ or -] 3.7 Meal frequency 7.8 7.5 6.5 [+ or -] 1.0 ** [+ or -] 1.3 ** [+ or -] 0.9 Night meals 0.3 0.3 0.3 [+ or -] 0.4 [+ or -] 0.5 [+ or -] 0.4 Weight 6.8 8.2 9.1 [+ or -] 0.9 ** [+ or -] 1.0 ** [+ or -] 1.1 * Controls 6 mo n=21 9 mo n=22 12 mo n=20 mean [+ or -]SD mean [+ or -]SD mean [+ or -]SD KJ 2935.7 3536.2 3673.4 [+ or -] 468.9 [+ or -] 652.2 [+ or -] 1342.7 Kcal 707.2 854.6 882.3 [+ or -] 110.1 [+ or -] 153.3 [+ or -] 323.2 Proteins (g) 17.5 26.7 30.8 [+ or -] 3.4 [+ or -] 8.6 [+ or -] 13.1 Energy % of 10.0 12.6 13.6 proteins [+ or -] 1.5 [+ or -] 1.6 [+ or -] 2.1 Fats (g) 29.2 33.0 35.6 [+ or -] 5.2 [+ or -] 8.9 [+ or -] 11.6 Energy % 37.5 34.4 34.5 of fats [+ or -] 4.9 [+ or -] 5.1 [+ or -] 4.0 Carbohydrates 91.6 108.2 120.5 (g) [+ or -] 18.0 * [+ or -] 19.3 [+ or -] 16.3 * Energy % of 51.2 51.0 49.8 carbohydrates [+ or -] 4.8 [+ or -] 5.2 [+ or -] 4.0 * Sucrose (g) 2.3 5 7.2 [+ or -] 3.2 [+ or -] 3.6 [+ or -] 4.3 Meal frequency 5.8 5.9 6.2 [+ or -] 0.8 [+ or -] 0.8 [+ or -] 0.9 Night meals 0.2 0.2 0.1 [+ or -] 0.4 [+ or -] 0.3 [+ or -] 0.2 Weight 8.0 9.3 10.1 [+ or -] 0.9 [+ or -] 1.0 [+ or -] 0.9 * p < 0.05; ** p < 0.01; ANOVA Table 3. Mutans streptococci (MS) colonisation at 6, 9, and 12 months of age in children with CFD. CFU values log transformed. CHD 6 mo n=11 9 mo n=8 MS detectable % 82 71 MS (CFU) mean[+ or -]SD 1.8[+ or -]1.6 1.8[+ or -]1.8 95% CI 0.7-2.8 0.13-3.5 MS (CFU) ratio of 0.14[+ or -]0.13 0.16[+ or -]0.17 TVC mean[+ or -]SD 95% CI 0.05-0.23 0.01-0.32 CHD Controls 12 mo n=10 6 mo n=22 MS detectable % 90 59 MS (CFU) mean[+ or -]SD 3.9[+ or -]3.2 1.7[+ or -]1.8 95% CI 1.6-6.2 ** 0.9-2.5 MS (CFU) ratio of 0.32[+ or -]0.27 0.14[+ or -]0.14 TVC mean[+ or -]SD 95% CI 0.13-0.51 ** 0.08-0.20 Controls 9 mo n=22 12 mo n=22 MS detectable % 77 54 MS (CFU) mean[+ or -]SD 1.6[+ or -]1.5 1.1[+ or -]1.2 95% CI 1.0-2.3 0.6-1.7 MS (CFU) ratio of 0.13[+ or -]0.12 0.10[+ or -]0.11 TVC mean[+ or -]SD 95% CI 0.08-0.18 0.05-0.14 (CFU = colony forming unit; TVC = total viability count) ** p < 0.01, ANOVA
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|Author:||Hansson, L.; Rydberg, A.; Stecksen-Blicks, C.|
|Publication:||European Archives of Paediatric Dentistry|
|Date:||Oct 1, 2012|
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