ABSTRACTSurveillance studies have shown that cleft lip and palate (CLP) is one of the commonest craniofacial anomalies (CFA), occurring in approximately 1 in 500 livebirths. Taking into consideration the world population and annual birth rates, it is estimated that there are well over a quarter million babies born each year with CLP. The cost of managing this huge number of clefts is enormous and exceeds the available resources of most developing countries in Asia, Africa and Latin America. Thus, CLP constitutes a major health problem which requires globally-based strategies to deal with the issues of epidemiology, primary prevention and treatment strategies which are evidence based and cost-effective. Basic research to unravel the aetiological factors responsible for clefting disorders is occurring on a worldwide scale, especially in the areas of molecular genetics and gene-environment interactions. There are also in place international organisations such as the WHO Task Force on CFA, the International Consortium on Oral Cleft Genetics (ICOCG), Interplast and other international volunteer cleft missions to help in the treatment of patients with cleft disorders in developing countries, in data collection, in pooling of genetic material and sharing of information. However, there is an urgent need for more randomised clinical trials (RCTs) to evaluate the outcomes of treatment so that clinical guidelines and treatment protocols are based on strong evidence. Currently, there is a dearth of RCT-based information and multicentre trials on treatment outcomes should therefore be actively pursued and encouraged.
I have chosen as the title of my keynote address “New Treatment and Research Strategies for the Improvement of the Care of Cleft Lip and Palate Patients”. The reason for this is that despite the tremendous strides we have made over the past 50 years in the management of cleft lip and palate (CLP), there are still wide gulfs in our knowledge and understanding of the embryogenesis of clefts and the causative factors responsible for CLP, especially the role of gene-environment interactions in non-syndromic clefts.
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