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Non-syndrome orofacial clefts: preventative measures
- Sameer Mallick, Butt MA, ST2 general medicine, Worthing Hospital (26 February 2008)
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Fissures of Lips and Palate
- Curbeira Hernández, Eduardo M, MSc MDD, Rosell Silva Clara. MDD, Acevedo Sierra Odalys. MDD, Hernández Fernández Juana. MSc (2 March 2008)
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Sameer Mallick, F1 elderly care medicine Worthing Hospital, West Sussex BN11 2DH, Butt MA, ST2 general medicine, Worthing Hospital
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The editorial by Lees suggests further epidemiological studies are needed to identify preventative measures to the development of congenital abnormalities such as orofacial clefts (OFC) [1]. The origin of non- syndrome clefts is likely to be multifaceted, involving both genetic and environmental factors. There is evidence that OFC may be associated with material deprivation [2]. In one study 65% of clefts occurred in individuals from a lower class background, 28% from middle class, and only 7% from those of upper class background. This finding was supported by a Welsh study in which a significant increase in the development of OFC’s in those who reside in the most deprived neighbourhoods was reported [3]. Increasing evidence also suggests an association between maternal nutrition and OFC. Opitz described its relationship with cholesterol [4], while Krapels et al commented on a correlation between OFC and reduced dietary intake of Vitamin B [5]. Deficiencies of minerals such as iron, zinc and magnesium were also found to be additional factors in Krapels study. Furthermore, there is some evidence for decreased OFC risk with increasing intakes of total protein, choline, methionine and cystiene [6]. Intake of iron and riboflavin was also found to reduce OFC risk when adjusted for other nutrients in this study. These nutrients are essential for palatogenesis. Availability of dietary advice in pregnancy regarding which foods contain good sources of these vitamins and minerals is therefore essential. Hypoxia during the first trimester may occur by temporary constriction of the uterine arteries. Drugs such as cocaine and nicotine have this effect. There is evidence that maternal exposure to such agents have resulted in hypoxia-related malformations such as OFC in humans [7]. Adequate counselling on the dangers of recreational drug use during pregnancy, including the dangers of smoking, is vital. Impaired glucose control in pregnancy may also contribute to development of OFC. In one study, diabetic mothers were found to be 1.352 times more likely than non-diabetic mothers to have a newborn with cleft lip or palate [8]. Obesity and a lack of physical exercise can amplify insulin resistance in pregnancy leading to the potential development of gestational diabetes. Studies have shown that regular physical activity before and during pregnancy can reduce the risk of gestational diabetes [9]. It is clear that the intricate genetic and environmental interactions in the development of OFC make the study of aetiological factors a challenging task. Nevertheless, the literature does describe some ‘preventative’ measures to help decrease the incidence of congenital abnormalities such as OFC. References 1. Lees M. Familial risks of oral clefts. BMJ. 2008; 336:399. 2. Sivaloganathan V. Cleft lips in Malaysians. Plast Reconstr Surg. 1972;49:176–9. 3. Durning P, Chestnutt IG, Morgan MZ, Lester NJ. The relationship between orofacial clefts and material deprivation in Wales. Cleft Palate Craniofac J. Mar 2007; 44(2):203-7. 4. Opitz JM, Gilbert-Barness E, Ackerman J, Lowichik A. Cholesterol and development: the RSH (“Smith- Lemli-Opitz”) syndrome and related conditions. Pediatr Pathol Mol Med. 2002;21:153–181. 5. Krapels IPC, van Rooij IALM, Ocke´ MC et al. Maternal dietary B vitamin intake, other than folate, and the association with orofacial cleft in the offspring. Eur J Nutr. 2004; 43:7–17. 6. Shaw GM, Carmichael SL, Laurent C, Rasmussen SA. Maternal nutrient intakes and risk of orofacial clefts. Epidemiology. May 2006; 17(3):285- 91. 7. Webster WS, Abela D.. The effect of hypoxia in development. Birth Defects Res C Embryo Today. Sep 2007; 81(3):215-28. 8. Spilson SV, Kim HJ, Chung KC. Association between maternal diabetes mellitus and newborn oral cleft. Ann Plast Surg. 2001; 47:477–481. 9. Damm P, Breitowicz B, Hegaard H. Exercise, pregnancy, and insulin sensitivity--what is new? Appl Physiol Nutr Metab. Jun 2007; 32(3):537-40. Competing interests: None declared |
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Curbeira Hernández, Eduardo M, MSc MDD, Dentistry Department “Dr. Gustavo Aldereguía Lima” University Hospital. cienfuegos, cuba. Postcode 55100, Rosell Silva Clara. MDD, Acevedo Sierra Odalys. MDD, Hernández Fernández Juana. MSc
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Congenital malformations are known since the very beginning of mankind , as it has been shown in small stamps and records of last civilizations which have been found in different countries of the world. Some scientists have considered that the labial-palatal fissure goes back to the year 2000 BC.
The birth of a malformed child has always caused sadness but the explanation of this phenomenon has changed from times to times according to the magic-religious, or philosophic concepts prevailing at the time. Thus, in some cultures a malformed child was not considered a pure infant and it was thought that this child should not live , being therefore destroyed whereas in others, this same phenomenon was adored and idealized. In some religions it was considered as a divine punishment and in some others it was considered as the announcement of a bad future event due to disagreement with God or due to Cosmic Wars. Due to the complexity of the deformity the patients can have with maxillofacial fissures, it is necessary to analyze this phenomenon with a multidisciplinary approach. In most of the cases treatment lasts about 18 years, since the moment of birth to the moment of the aesthetical surgery, although in some cases it lasts the whole life as it happens in the case of the installation of obstructers Epidemiology of the labial-palatal fissure The average of major congenital malformations at the moment of birth is about 3 % if we only consider alive newborns. This frequency increases if we consider miscarriages, abortion or deaths. The labial-palatal fissures are among the commonest anomalies . In a Latin American collaborative study of Congenital Malformations during the period 1982-1990 a global rate of 10,49 × 10 000 for cleft lip was found, calling the attention the high frequency found in Bolivia (23,7), Ecuator (14,96) and Paraguay (13,3), probably due to the fact that their populations have a mixture of the Indian race. However, lower rates were found in Venezuela (7,92), Perú (8,94), Uruguay (9,37) y Brasil (10,12), every 10 000 inhabitants , fact which is explained by the mixture of these populations with the black race It has been stated that the whole incidence of maxillofacial fissures comprises between 1:500 y 1:700 births ,3,6,7 although in the latest years due to the birth control and the genetic assessment the 9incidence of these fissures have diminished. The commonest parts compromised by oral fissures are the upper lip, the alveolar border, the hard and the soft palates . Slightly most of the 50% are combined lip-palate fissures and about a quarter of them is bilateral . The isolated fissures of lips and palate constitute the remaining types present in our cases. It has been proven that the fissures of the lips are more frequent in males meanwhile isolated fissures of the palate are more common in females. The compromise of fissured lip is most frequent in the left than in the right side. This phenomena is under study and up to the present it lacks of explanation and the underlying cause of the deformity is partially understood. The lack of conjunction between the parts that form the lip and the palate is formed in an early stage of the foetal life. Bibliography 1. Leez M. Familial risks of oral clefts. BMJ 2008;336:399 2. Coiffman F. Texto de cirugía plástica, reconstructiva y estética. La Habana: Editorial Científico-Técnica; 1986. 3. Pantoja R, Cauvi D, Cortes J, Argandoña J. Cirugía ortognática en fisurados. Rev Esp Cir Oral Maxilofac 1997;19(2):100-4. 4. Collares M, Weestphalen A, Costa TC, Goldin JR. Fisuras labio-palatinas: incidencia e prevalencia de patología no Hospital de Clínicas de Porto Alegre: un estudio de 10 años. Rev AMRIGS 1995;39(3):183-8. 5. Nazer Herrera J, Villa Vicent JJ, Van Deer Baars Moreno R, Cifuentes Ovalle L. Incidencia de labio leporino y paladar hendido en latinoamérica: período 1982-1990. Pediatría 1995;37(1-2):13-9. Competing interests: None declared |
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