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Cigarette smoking and orofacial cleft development: dental hygiene's role in education and prevention.

Cleft lip with or without cleft palate is one of the most common cranial malformations seen worldwide. (1) The purpose of this article is to inform and educate the dental hygienist regarding the formation of the lip and palate, genetics and gene-environment interactions, and the effects of maternal smoking. In addition, the presurgical orthopedic appliance, a treatment option used to correct orofacial clefts, is presented and illustrated. At the conclusion of this article, a discussion including ideas and information that dental hygienists can use to help facilitate patient smoking cessation is presented.

For years, public awareness campaigns initiated by the Surgeon General's warnings have informed the public about the respiratory and cardiac ramifications of smoking. (2) Unfortunately, information explaining why and how the chemicals in cigarettes could possibly affect lip and palate formation have not been well publicized. (3) As more research is conducted, the general public will need to become aware of the dangers of tobacco smoke and the detrimental effect it has on developing embryos. The dental hygiene and dental community, with support from its professional organizations, is in a unique position to educate the public.

As more research is conducted, the general public will need to become aware of the dangers of tobacco smoke and the detrimental effect it has on developing embryos. The dental hygiene and dental community, with support from its professional organizations, is in a unique position to educate the public.

Types of Cleft

Cleft lip with or without cleft palate occurs in approximately 1 out of 700 live births worldwide. (1,4) This type of orofacial cleft involves "structures anterior to the incisive foramen, including the lip and alveolar ridge," (1) which make up the primary palate. The primary palate forms independently from the secondary palate between weeks four and six of pregnancy. Orofacial clefts are the result of the medial nasal prominences failing to fuse and merge with the maxillary prominences. The failure to fuse can be expressed unilaterally or bilaterally. (1,4)

Clefting of the secondary palate only includes all structures posterior to the incisive foramen. This type of cleft is seen in one out of 2,500 live births. The secondary palate fuses between weeks eight and twelve of pregnancy and, as seen with the primary palate, failure to fuse results in the formation of a secondary cleft palate. (1,4)

Treatment of Orofacial Clefts

In 2004, Johansson and Ringsberg reported in the Journal of Advanced Nursing the results of their study focusing on the available medical and psychological support for families experiencing orofacial clefts. The study, conducted in Sweden, focused on the effectiveness of a craniofacial team that was available to parents whose children were born with an orofacial cleft. The purpose of the craniofacial team was to offer help and practical information regarding future surgical and restorative plans. The team consisted of a physician, speech therapist and dentist. Participants felt the team approach was helpful and suggested adding a psychologist to help them discuss their feelings. (5)

When interviewed for this article, Tim Henson, DMD, associate professor and postdoctoral program director in the Department of Pediatric Dentistry at the University of Texas Health Science Center at San Antonio Texas and member of the Craniofacial Anomalies Team at Christus Santa Rosa Children's Hospital in San Antonio, emphasized that the team approach is vital for the care of an infant born with an orofacial cleft. A plastic surgeon at Christus Santa Rosa Hospital leads the team consisting of Henson; an orthodontist; a pediatric ear, nose and throat specialist; speech and hearing specialists; geneticists; a psychologist and a social worker. All of the health care providers meet with the parents and infant to completely evaluate the baby's physical and genetic health and provide services for the parents' mental health and well being. Based on his experience, Henson said, "The psychological and social work aspect of the team is important. There are often cultural stigmas that need to be addressed along with some sense of guilt. Many parents ask, 'What did I do wrong?' The psychologists and social workers can help the parents overcome those feelings."

One of the treatments provided by the Craniofacial Anomalies Team involves the use of a presurgical orthopedic appliance. The parents meet with Henson prior to the baby's birth to discuss the orofacial cleft development and treatment process. Once the new born is five to seven days old and in good health, Henson takes impressions of the maxilla and constructs the appliance that will be placed in the infant's mouth to move the alveolar ridge and lip tissue in preparation for surgery (figures 1 and 2). The parents must take the appliance out four to six times per day over the next three months to clean it. In addition, Henson must examine the infant and adjust the appliance weekly until the baby is approximately three months old. Henson said, "Parents get very exasperated with the process of removing the orthodontic bands and steri-strips holding the appliance in the mouth, cleaning it and then putting the appliance back in place. The learning curve is big, especially during the first week. Parents must be comfortable with the process for it to work, so we make sure parents have the ability to contact the team whenever they need to. We must act as a shoulder for parents to cry on at times." After three months, the infant will have plastic surgery to close the lip and make any needed adjustments to the nose (figures 3 and 4). At 10 months of age, the baby undergoes bone graft surgery to close the palatal cleft. Typically, the presurgical orthopedic appliance has reduced the surface area of the cleft, thus making the graft smaller. Finally, Henson stresses that the goal of the treatment process is to reduce the number of surgeries and facial scarring for the infant through the use of the presurgical orthopedic appliance (figure 5).






Public Perceptions and Awareness

Maternal attitudes toward smoking and orofacial cleft formation are discussed throughout the literature. In a 2004 article in Epidemiology, Meyer et al. report on their study conducted in Sweden. They found that most mothers who smoked during their pregnancy and gave birth to children with orofacial clefts would continue to smoke if they decided to conceive again. (3) In another 2005 study, published in the Bulletin of the World Health Organization, Little et al. discuss their meta-analysis and find a "consistent, moderate and statistically significant association between maternal smoking and deft lip, with or without cleft palate" formation. Little suggests that the evidence correlating smoking and orofacial cleft development is strong enough to justify its use in anti-smoking campaigns.' In yet another article, published in The Cleft Palate-Craniofacial Journal in 2003, Little et al. examine the lack of public knowledge regarding smoking and orofacial cleft development using a case-control study. Within that study, Little discloses that The World Health Organization neglected to include information on orofacial cleft formation associated with maternal smoking in their 2001 report on women and the tobacco epidemic/Clearly, there is a need to analyze how the public is reached with tobacco cessation information and from that analysis develop effective modes of information dissemination.

Current Studies Associating Smoking with Orofacial Clefts

The most current research on orofacial cleft development is focused in two areas: genetics and experimental research. Geneticists are studying the chromosomes, searching for specific markers that may lead to orofacial cleft formation. (4) Some researchers are focusing on the direct effect that toxic chemicals, such as those found in cigarette smoke, have at the cellular level. (8,10) Other researchers are examining the gene-environment link, which includes cigarette smoking and the formation of orofacial clefts. (8,11,16)

Genetic Research

For years, genetic researchers have explored the idea of heredity as a possible risk factor in the formation of orofacial clefts. (4) In the March 2003 issue of The Journal of Craniofacial Surgery, Carinci et al. found, out of 23 pairs of chromosomes, loci on chromosomes 2, 4, 6, 11, 17, and 19 that are factors in orofacial cleft development? Chromosome number 4 has markers on it that play a role in orofacial cleft formation, especially when combined with environmental factors such as cigarette smoking or alcohol consumption? The authors state at the conclusion of their article that more research is necessary to continue the isolation of specific genes or sites on genes that could be responsible for orofacial cleft formation. (4)

Experimental Research

The current experimental research focuses on two topics: toxins in cigarettes and their direct effect at the cellular level during embryonic development, and the gene-environment link aiding in the expression of existing genetic tendencies for the development of orofacial clefts.

In a study conducted by Saito et al. in 2005 and published in Toxicology, the effects of N'-nitrosonornicotine (NNN), which is a "tobacco-specific nitrosamine," (8) are explored and discussed in great detail. The study focuses on the pathways hypothesized to be involved in the disappearance of the palatal shelf medial edge epithelium during embryonic development. All embryonic parts of the future skeleton follow a developmental sequence that can be easily disrupted. The medial edge epithelial cells play an important role in the adherence and fusion of the two palatal shelves. For the fusion process to be complete, cellular apoptosis or death of the medial edge epithelium must take place. (8) The two pathways involved with apoptosis of the medial edge epithelium are EGF (epidermal growth factor) and transforming growth factor-beta. These pathways are thought to play key roles in cell proliferation and differentiation, and Saito's study observed NNN disrupting those pathways. (8)

The idea of a gene-environment interaction involved in orofacial cleft development has been explored in several studies. The results of a 2005 study by Shaw, et al., published in the American Journal of Epidemiology, found an increase in orofacial cleft development when the infant carried a genetic variation affecting nitric oxide synthase and the mother smoked and did not take prenatal vitamins, specifically folic acid. It is documented in this study that smoking compromises endothelial nitric oxide synthase and that, combined with a genetic variation in the mother and/or infant, it resulted in the formation of an orofacial cleft. (12)

In addition to studying the effects of chemicals found in cigarette smoke, Lammer et al. (2005) published an article in Epidemiology examining the risk of developing orofacial clefts in embryos lacking the genetic ability to produce enzymes that detoxify chemicals found in cigarette smoke. A specific enzyme, glutathione-S-transferase, makes toxic chemicals more water-soluble so they can be excreted by the body. Lammer's study suggests that the risk for orofacial clefts increases almost seven times the average rate when the mother is a heavy smoker (defined as 20 or more cigarettes per day), and the embryo lacks the gene to produce glutathione-S-transferase. For embryos who lack glutathione-S-transferase and whose mother smoked fewer than 20 cigarettes per day, the average risk for orofacial cleft development is approximately three times the average rate of occurrence. (9)

In a 2001 article in Epidemiology, vanRooij et al. suggest that the susceptibility of the embryo to cigarette smoke depends on biotransformation of the toxic compounds contained within the smoke. These researchers found that cigarette smoke toxins directly affect the embryo in three ways. First, the chemicals can damage the developing tissue by creating a hypoxic, or oxygen-poor environment for the embryo. Second, carcinogens can be passed along to the embryo, binding DNA. Some toxins are excreted in the urine; however, fat-soluble chemicals are stored in fatty tissue and then released at a later date. The maternal biotransformation of the toxins can be absent or highly active depending on genetic variations. Third, combinations of biotransformation pathways can result in tissue exposure and damage. The study by vanRooij points to smoking as part of a process that includes genetic variation resulting in increased risk for orofacial cleft development. (10) In addition, Lorente et al. published an article in 2000 in the American Journal of Public Health highlighting the relationship between smoking and orofacial clefts. Lorente obtained data from a European multicenter case-control study and, through multivariate analyses, determined that environmental exposures to tobacco and alcohol play a role in the development of orofacial clefts. (13)


Not all orofacial clefts are caused by smoking. Rather, most studies have determined that cigarette smoke, directly or indirectly, affects tissue development in combination with genetic interaction. The messages found in the reviewed studies highlight the serious implications of exposing the developing embryo to toxic chemicals. The important result from the research is the need to further study and understand the role tobacco chemicals play in the development of orofacial malformations.

A Dental Hygienist's Role

So how does the dental hygienist's role serve to promote oral health, minimize disease and educate the public on the toxic effects of cigarette smoke on developing embryos? As preventive professionals, dental hygienists are in an instrumental position within the entire health care system to address concerns about smoking and its effects on a developing embryo. With various continuing education courses available, dental hygienists can acquire a vast amount of valuable information that can be passed on to patients. For instance, it is important to note and share with patients that cigarette smoke contains 55 carcinogens that could harm the individual and a developing embryo. (16) It is vital for dental hygienists to become familiar with the stages of embryonic development and the possible toxic effects of cigarette smoke at these stages. Women may feel more confident about the information presented to them if the dental hygienist is educated on the topic and can articulate the information clearly.

In both the clinical and community settings, women of child-bearing age who smoke must be provided with education explaining orofaciat cleft formation. Patient education brochures providing a how-to guide to tobacco cessation information; photographs and description of palate formation; and the effects of smoking, alcohol consumption, lack of folic acid and other environmental factors would be beneficial to review with patients. Along with information describing orofacial cleft formation, the surgical correction process, dental implications and long-term possible psychosocial effects need to be brought to the woman's attention. If clear and concise education is provided by the dental hygienist, women may have current information to make a decision to quite smoking. Behavior modification can be extremely challenging; however, the knowledge that a child's well being is at stake may serve as incentive for smoking cessation.

To complete the information process it is important for dental practices and community health centers to have the necessary information explaining smoking cessation programs utilizing evidence-based tobacco cessation tool kits. In addition, in providing information to patients, dental hygienists need to establish a working relationship with local physicians and counselors who can help provide care to patients who do not have their own physician or counselor to guide them through the smoking cessation process. Dental hygienists and dentists can collaborate to involve community organizations or women's public health centers to disseminate information. Public service announcements sponsored by the American Dental Hygienists' Association or the American Dental Association may reach a wide and diverse audience. While not all orofacial clefts are caused by smoking, it is vitally important that, as oral health care providers, we insure patients receive the most appropriate information and care possible to reduce the number of infants born with orofacial deformities.


The photographs that accompany this article appear courtesy of Timothy B. Henson, DMD, assistant professor and postdoctoral program director in the department of Pediatric Dentistry at the University of Texas Health Science Center at San Antonio.


(1.) Stroustrup-Smith A, Estroff JA, Barnewolt CE, et al. Prenatal diagnosis of cleft lip and cleft palate using MRI. Am J Roentgenol 2004; 183:229-35. Available at cgi/content/full/183/1/229?maxtoshow=&. Accessed Oct. 19, 2005.

(2.) U.S. Department of Health and Human Services. Reducing tobacco use: a report of the Surgeon General. Fact Sheet, 2005. Atlanta: U. S. Department of Health and Human Services, Centers of Disease Control and Prevention. Available at

(3.) Meyer KA, Williams P, Hernandez-Diaz S, Cnattingius S. Smoking and the risk of oral clefts: exploring the impact of study designs. Epidemiol 2004; 15, 671-8. Retrieved from Ovid Oct. 13, 2005.

(4.) Carinci F, Pezzetti F, Scapoli L, et al. Recent developments in orofacial cleft genetics. J Craniofacial Surg 2003; 14: 130-43. Retrieved from Ovid Oct. 13, 2005.

(5.) Johansson B, Ringsberg K. Parent's experiences of having a child with cleft lip and palate. J Advanced Nurs 2004; 47: 165-73. Retrieved from Ovid Oct. 25, 2005.

(6.) Little J, Cardy A, Munger RG. Tobacco smoking and oral clefts: a meta-analysis. Bull World Health Organ 2004; 82: 213-8. Retrieved from Ovid May 23, 2006.

(7.) Little J, Cardy A, Arslan MT, et al. Smoking and orofacial clefts: a United Kingdom-based case-control study. Cleft Palate-Craniofacial J 2003; 41: 381-6. Retrieved from Medline Oct. 7, 2005.

(8.) Saito T, Cui XM, Yamamoto T, et al. Effect of n'-nitrosonornicotine (NNN) on murine palatal fusion in vitro. Toxicol 2005; 207: 475-85. Retrieved from Science Direct Oct. 7, 2005.

(9.) Lammer EJ, Shaw GM, Iovannisci DM, Finnell RH. Maternal smoking, genetic variation of glutathione s-transferases, and risk for orofacial clefts. Epidemiol 2005; 16: 698-701. Retrieved from Ovid Oct. 13, 2005.

(10.) van Rooij I, Wegerif M, Roelofs H, et al. Smoking, genetic polymorphisms in biotransformation enzymes, and nonsyndromic oral clefting: a gene-environment interaction. Epidemiol 2001; 12: 502-7. Retrieved from Ovid May 23, 2006.

(11.) Bille C, Knudsen L, Christensen K. O. Changing lifestyles and oral clefts occurrence in Denmark. Cleft Palate-Craniofacial J 2004; 42: 255-9. Retrieved from Ovid Oct. 7, 2005.

(12.) Shaw GM, Iovannisci DM, Yang W, et al. Endothelial nitric oxide synthase (NOS3) genetic variants, maternal smoking, vitamin use, and risk of human orofacial clefts. Am J Epidemiol 2005; 162: 1207-14. Retrieved from Medline May 26, 2006.

(13.) Lorente C, Cordier S, Goujard L, et al. Tobacco and alcohol use during pregnancy and risk of oral clefts. Occupational Exposure and Congenital Malformation Working Group. Am J Public Health 2000; 90: 415-9. Retrieved from Ovid May 23, 2006.

(14.) Wyszynski DF, Wu T. Use of US birth certificate data to estimate the risk of maternal cigarette smoking for oral clefting. Cleft-palate-Craniofacial J 2002; 39: 188-92. Retrieved from Ovid May 23, 2006.

(15.) Lieff S, Olshan AF, Werler M, et al. Maternal cigarette smoking during pregnancy and risk of oral clefts in newborns. Am J Epidemiol 1999; 150: 683-94. Retrieved from Ovid May 23, 2006.

(16.) Hartsfield JK, Hickman RA, Everett ET, et al. Analysis of the EPHX1 113 polymorphism and GSTM1 homozygous null polymorphism and oral clefting associated with maternal smoking. Am J Med Genetics 2001; 102: 21-4. Retrieved from Medline May 23, 2006.

Magda A. de la Torre, RDH, BS, MPH, is presently an assistant professor in the Department of Dental Hygiene at the University of Texas Health Science Center at San Antonio (UTHSCSA). She worked numerous years in private practice, received her RDH and BS degrees from the UTHSCSA and her MPH from Texas A&M University, School of Rural Public Health. She currently is the program director for Building Oral Health Care Access (BOHCA), a community service-learning program along the Texas-Mexico border region. The program provides dental hygiene students the opportunity to learn about cultural competency and social responsibility.

Michelle A. Thurman, RDH, BSDH, graduated with honors from the University of New Mexico Department of Dental Hygiene with an Associate of Science degree in Dental Hygiene in 1993. After graduation, she worked with general dentists in New Mexico and Texas. She graduated with honors from the University of Texas Health Science Center at San Antonio in December 2006 with a Bachelor of Science degree in Dental Hygiene. She currently works part-time with John B. Durnford, DDS in Schertz, Texas.
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Title Annotation:clinical feature
Author:de la Torre, Magda A.; Thurman, Michelle A.
Geographic Code:1USA
Date:Jan 1, 2008
Previous Article:Observations outside the oral cavity for effective patient care.
Next Article:Symposia highlight oral-systemic link.

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