Cigarette Smoking and the Impact on Cleft Lip

Cigarette Smoking and the Impact on Cleft Lip

Law firms around the country are investigating cases involving certain medications and the development of cleft lip and cleft palate in new borns. There has been quite a bit of research done regarding clp and the various factors that can contribute to birth defects. One interesting study is called, "Cigarette smoking as an etiologic factor in cleft lip and palate.Ericson A, Klln B, Westerholm P." Am J Obstet Gynecol. 1979 Oct 1;135(3):348-51. Here is an excerpt: "Abstract - A case-control study has been made on smoking habits in women who, during 1975, gave birth to infants with closure defects of the central nervous system (ASB) or with cleft lip or cleft palate (CLP). For each case, two control subjects with nonmalformed infants were selected and matched for delivery unit, time of delivery, maternal age, and maternal parity. Smoking habits were routinely included in hospital records at first visit to a maternity health clinic during pregnancy. Data were studied for 66 cases of CLP, 66 cases of ASB, and 261 control subjects. Significantly more women who had infants with CLP smoked than did control women, but women with ASB infants showed a normal smoking pattern. Drug use did not explain the findings. It is suggested that maternal smoking is one of many factors of importance in the etiology of cleft lip and cleft palate in humans."

Another interesting study is called, "A Preliminary Study of Facial Growth and Morphology in Unoperated Male Unilateral Cleft Lip and Palate Subjects Over 13 Years of Age" by Michael Mars, F.D.S., D.Orth. and William J. B. Houston, F.D.S., Ph.D. Michael Mars and William J. B. Houston (1990) The Cleft Palate-Craniofacial Journal: January 1990, Vol. 27, No. 1, pp. 7-10. Here is an excerpt: "Abstract - This paper investigates the effects of surgery on facial growth and morphology in Sri Lankan males with unilateral cleft lip and palate who were over 13 years of age at the time of study with cephalometry and dental study models. Three separate subgroups were analyzed: those who had totally unrepaired cleft lip and palate, those who received lip repair in infancy but not palatal repair, and those who had lip and palate repair in infancy. Twenty-three healthy noncleft Sri Lankan males over 13 years formed a control group from the same racial background. The results show that subjects who had no surgery had a potential for normal maxillary growth. Subjects who have had lip repair in early infancy show relatively normal maxillary growth, but maxillary hypoplasia is common when the palate has also been repaired early."

Another interesting study is called, "Mutations of PVRL, encoding a cell-cell adhesion molecule/herpesvirus receptor, in cleft lip/palate-ectodermal dysplasia" by Koji Suzuki, Diane Hu, Tania Bustos, Joel Zlotogora, Antonio Richieri-Costa, Jill A. Helms & Richard A. Spritz - Nature Genetics 25, 427 - 430 (2000). Here is an excerpt: "Cleft lip, with or without cleft palate (CL/P), is one of the most common birth defects, occurring in 0.4 to 2.0 per 1,000 infants born alive1. Approximately 70% of CL/P cases are non-syndromic (MIM 119530), but CL/P also occurs in many single-gene syndromes, each affecting a protein critical for orofacial development. Here we describe positional cloning of the gene responsible for an autosomal recessive CL/P-ectodermal dysplasia (ED) syndrome (CLPED1; previously ED4; ref. 2), which we identify as PVRL1, encoding nectin-1, an immunoglobulin (Ig)-related transmembrane cell-cell adhesion molecule that is part of the NAP cell adhesion system3, 4, 5, 6. Nectin-1 is also the principal cell surface receptor for -herpesviruses (HveC; ref. 7), and the high frequency of CLPED1 on Margarita Island in the Caribbean Sea might result from resistance of heterozygotes to infection by these viruses."

We all owe a debt of gratitude to these researchers for their fine work and dedication. For more information, please read the studies in their entirety.

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