Fluoride Action Network

Abstract

As a consequence of chronic renal failure (CRF) and its treatment, a number of oro-dental changes occur that persist after the end-stage is reached. An early effect is enamel hypoplasia due to a defect of enamel development and mineralisation. This is usually reparable to a high aesthetic standard using dental composite filling material. Children with CRF have significantly less dental caries than healthy children due to the inhibitory effect of increased salivary urea levels. Grafted patients frequently develop gingival enlargement as a result of immunosuppression with cyclosporine A, which is further exacerbated by the additional use of antihypertensive calcium-blocking agents. Surgical reduction of gingival hyperplasia is effective and is required in approximately one third of adolescents. A very high standard of home care should be encouraged for all children with CRF in the form of thorough mechanical tooth cleaning and plaque inhibition through the use of an antibacterial mouthwash. In transplanted children presenting an increased risk of infection, antibiotic prophylaxis may be indicated for dental treatment procedures. The drug dosage should be adapted to the reduced renal function. Pediatric nephrologists should be aware that dental surgeons can make a considerable contribution to the general health and well-being of children with CRF. Thus, only oro-dental problems that are mainly encountered and treated by dental surgeons are reviewed.

Excerpt:

Enamel hypoplasia

 

The pathogenesis of this is that severe metabolic upset causes a permanent mark, called enamel hypoplasia, in the developing tooth which remains as a visible defect on the tooth throughout the life of the patient. The position and extent of the defect indicates the timing, duration and to some extent the severity of the underlying metabolic upset. Enamel hypoplasia is frequently seen in patients with renal disease, and has been attributed to the production of poorly-formed enamel as a result of ameloblast disruption (Figs. 3 and 4). Factors responsible for this disruption include hypocalcaemia, decreased serum levels of 1,25-dihydroxycholecalciferol, and raised serum levels of inorganic phosphate and serum parathyroid hormone. An elevated serum fluoride level, causing fluorosis, may be an aetiological factor in the development of enamel defects in children with CRF, since the kidneys have an important function in the removal of inorganic fluoride from the body. In children, enamel hypoplasia was observed in 26 of a group of 50 children (52%) with CRF. Other workers concluded that the onset of renal disease leading to CRF in the first few weeks of life may effect enamel formation in primary teeth early in postnatal life. The lesions recorded differed from those seen in the permanent dentition. Other workers observed severe enamel hypoplasia in both the primary and permanent teeth of a group of 38 children with end-stage renal failure.

The studies quoted have reported up to 22%, 34%, 50% and 57% of patients affected with clinically unsightly enamel hypoplasia. This is important, as it represents a burden of dental care that will usually require the techniques of aesthetic dentistry to improve the appearance. Children and adolescents become increasingly aware of their appearance as they mature, so the request for an improvement in appearance may come in the early years of the second decade of life. This should be factored into the cost of setting up a pediatric renal unit with appropriate support services. An emerging concern is the possible effect on the development of dental caries. As indicated below, children who receive transplants that are deemed successful show changes in salivary composition to normality. This may put the children with successful transplants at a slightly greater risk of developing dental caries. This is because hypoplastic pits and groves on the tooth surface enable the accumulation of bacterial plaque and may become carious because of the difficulty in removing bacterial plaque that has accumulated in the hypoplastic areas.