The reported association between chronic malnutrition, growth, and dental caries suggests that dental decay might contribute to poor weight gain in children (Alvarez et al, 1990). Four cases of children with early childhood caries and subsequent dental rehabilitation were published by Acs in 1998 (Acs et al, 1998). Regardless of the presumptive aetiology of the poor weight gain, all of these children demonstrated an immediate increase in weight, propelling them to higher weight percentile categories with increased adjusted 6-month increments of growth after their carious teeth had been repaired. At the end of the observation, none of these children continued to satisfy the criteria for the designation of faltering growth. These observations were consistent with the phenomenon of catch-up growth that has been observed in faltering growth children (Prader et al, 1963).
The effect of dental health improvement on growth was evaluated through another study by Acs in 1999 (Acs et al, 1999). The percentile weight categories of children with non-contributory medical histories and early childhood caries were compared to caries free patients, before and after comprehensive dental treatment under general anaesthesia. Percentile weight categories of the test subject were significantly less than that of the comparison group and 13.7% of ECC patients weighed less than 80% of their ideal weight. Following complete dental rehabilitation, children with ECC exhibited significantly increased growth velocities through the course of the follow-up period. At the end of the follow-up period there were no longer any statistically significant differences in the percentile weight categories of the test and comparison groups.
In a longitudinal clinical trial study in Manchester treatment of severe caries resulted in weight gain in 5-6 year-old children. (Malek Mohammadi et al, 2009) One thousand two hundred children aged 2-12 year-old had carious teeth extracted under general anesthesia during the study period. Of these, 218 five and six year old children participated in the study. Most of the children recruited to the study had a high caries rate, as expected. The mean (SD) dmft was 7.18 (3.27). Fifty-eight per cent of children had dmft >6. Ninety-six (44%) children had signs of dental abscesses or oral fistula when they were examined. The children as a group were of average height, weight and BMI. The proportion of the study population who weighed below the standards tenth percentile at baseline was 6.9% (15), whilst 8.3% (18) were below the standard's 10th percentile for height. Frequency distribution of the study population's weight, height and BMI at baseline and follow up indicated a decrease in the proportion of children in the lower percentiles for BMI, six months after extraction of carious teeth. On average the children showed a clear gain in weight at follow up and a slight gain in height. The 15 children with low weight (<10th percentile) at baseline also had significant increases in SD scores for weight and BMI (p<0.001) at follow up.
These studies suggest that children's ability to gain weight may be negatively affected by the presence of carious teeth in their mouths and that weight is gained more quickly than normal in the six months after tooth extractions.
In another longitudinal birth cohort, children who had caries at 61 months had slower increases in weight and height between birth and 61 months than those without decay at 61 months (Kay et al, 2010). It is possible that the chronocity of ECC may have a similar influence like other chronic diseases on a child, making them unable to sustain normal growth, and therefore, impacting on general health and well being.
Whilst nutrition is very important in growth and development, recently it has been suggested that children who do not have any medical problems, but who are deficient in growth, may have higher levels of caries. Growth deficiency and ECC may therefore be related in some way. Oral health affects people physically and psychologically and influences how they grow, enjoy life, look, speak, chew, taste food and socialize, as well as their feelings of social well-being (Locker, 1997).
If dietary intake alters as a result of caries this could result in an alteration of established growth patterns which are then re-established once the carious teeth are removed. The potential for increased glucocorticoid production in response to pain, decreased growth hormone secretion in response to disturbed sleep pattern, and overall increased metabolic rate during the course of infection are all possible explanations of the observed association between growth and caries. An alternative explanation for the observation would be that pain and infection alter eating habits e.g. if carious teeth become pulpitic, the eating of refined carbohydrates will cause pain and children may avoid such foods resulting in reduced calorific intake. Whichever explanation is accepted for the observed association, the hypothesis that dental disease and growth are related through the common factor of diet are supported by the studies presented and also seem plausible, both biologically, and behaviorally.
Severe caries detracts from children's quality of life: they experience pain, discomfort, disfigurement, acute and chronic infections, and eating and sleep disruption as well as higher risk of hospitalization, high treatment costs and loss of school days with the consequently diminished ability to learn. Caries may also affect nutrition, growth and weight gain. Children of three years of age with nursing caries weighed about 1 kg less than control children probably because toothache and infection alter eating and sleeping habits, dietary intake and metabolic processes. Disturbed sleep affects glucosteroid production (Acs, 1992).
Dental problems which cause chewing to be painful may affect the intake of dietary fibre and some nutrient-rich foods; consequently, serum levels of beta carotene, folate and vitamin C have been observed to be significantly lower in those with poorer oral status (Sheiham & Steele, 2001).
It is likely that younger children, with early caries, prior to the onset of pain and infection have poor feeding habits, particularly high carbohydrate intake. However as the children age and caries progresses, the onset of pain and infection may alter eating habits eg. If carious teeth become pulpitic, the eating of refined carbohydrates will cause pain and the child would therefore be more likely to avoid such foods. Altered dietary intake secondary to pain could therefore result in an alteration of established growth patterns.
Because oral and other chronic diseases have determinants in common, more emphasis should be on the common risk factor approach. The hypothesis that ECC and growth may be related through the common factors of diet and nutrition seems plausible. While there are many studies which have investigated the role of diet in children's growth and in dental caries, diet as a common casual factor for poor growth and dental caries has not previously been fully investigated.
Dental caries, which is associated with what children eat, poses a real, and potentially life threatening danger to the children affected by it, because it frequently results in general anaesthesia quite apart from any other effects it may have on child wellbeing. Diseases which do not cause small children to undergo general anaesthesia and all the risks and problems it entails, but which affect individuals' health many years later cause disquiet amongst nutritionists and paediatricians. It is unfortunate that a disease such as dental caries, which causes extreme pain and leads to outpatient general anaesthesia, does not seem to engender the same levels of worry and concern. It would seem that the impact of the caries on children's general health and well-being has largely been ignored.
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