- Email: [email protected]
HPV AND ORAL HEALTH: Response from Drs. Syrjanen and Rautava
COMMENTARY
LETTERS
such as tobacco-use cessation and limiting alcohol use. Jennifer L. Cleveland, DDS, MPH Dental Officer and Epidemiologist
Michele L. Junger, DDS, MPH Dental Public Health Resident Division of Oral Health
Mona Saraiya, MD, MPH Medical Epidemiologist Division of Cancer Prevention and Control National Center for Chronic Disease Prevention and Health Promotion
Lauri E. Markowitz, MD
www.cdc.gov/mmwr/preview/mmwrhtml/ mm5920a4.htm. Accessed March 29, 2012. 4. Smith EM, Rubenstein LM, Haugen TH, Hamsikova E, Turek LP. Tobacco and alcohol use increases the risk of both HPV-associated and HPV-independent head and neck cancers. Cancer Causes Control 2010;21(9):1369-1378. 5. Fiore MC, Jaén CR, Baker TB, et al. Treating Tobacco Use and Dependence: 2008 Update—Clinical Practice Guideline. Rockville, Md.: U.S. Department of Health and Human Services, Public Health Service; 2008. www.surgeongeneral.gov/tobacco/ treating_tobacco_use08.pdf. Accessed March 29, 2012. 6. D’Souza G, Agrawal Y, Halpern J, Bodison S, Gillison ML. Oral sexual behaviors associated with prevalent oral human papillomavirus infection. J Infect Dis 2009;199(9): 1263-1269. 7. Kreimer AR, Villo A, Nyitray AG. The epidemiology of oral HPV infection among a multinational sample of men. Cancer Epidemiol Biomarkers and Prevention 2011; 20(1):172-182.
1. Glick M, Johnson N. Oral and oropharyngeal cancer: what are the next steps (editorial)? JADA 2011;142(8):892-894. 2. Centers for Disease Control and Prevention. FDA licensure of Quadrivalent Human Papillomavirus Vaccine (HPV4, Gardasil) for use in males and guidance from the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2010;59(20):630-632. www.cdc.gov/mmwr/ preview/mmwrhtml/mm5920a5.htm. Accessed March 29, 2012. 3. Centers for Disease Control and Prevention. FDA licensure of Bivalent Human Papillomavirus Vaccine (HPV2, Cervarix) for use in females and updated HPV vaccination recommendations from the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2010;59(20):626-629.
Response from Drs. Syrjanen and Rautava: We want to thank Dr. Fleisher for raising important questions concerning our article. Human papillomavirus (HPV) and oral squamous cell carcinoma (OSCC) has been a controversial issue since the first evidence was presented by us in 1983.1 As discussed, this is partly because of the wide variation in HPV detection rates.2 A recent meta-analysis of case-control studies confirmed that it is nearly fourfold more likely to find HPV DNA in oral cancer than in the control samples.3 However, to prove HPV as a cause of oral cancer, additional evidence is requested, summarized as “modified Koch’s postulates,” as follows: dviral infection precedes the development of cancer, which has not yet been formally shown, although the metaanalysis mentioned above gives the best evidence available to date to this notion3; dviral genome presents in tumor lesions or in tumor cells, which has been clearly confirmed; depidemiologic association between presence of the virus and development of cancer has not been shown because no ran-
442 JADA 143(5)
May 2012
Medical Epidemiologist
Eileen F. Dunne, MD, MPH Medical Epidemiologist Division of Sexually Transmitted Disease Prevention National Center for Hepatitis, HIV/AIDS, Sexually Transmitted Diseases, and Tuberculosis Prevention Centers for Disease Control and Prevention Atlanta
Joel B. Epstein, DMD, MSD, FRCD(C), FDS RCS(Edin) Director, Oral Medicine Adjunct Professor Division of Head and Neck Surgery City of Hope, Duarte, Calif. and Medical-Dental Staff Clinician Cedars-Sinai Medical Center Los Angeles
http://jada.ada.org
domized case-control or cohort studies have been published; dthe virus or viral proteins are able to transform cells in vitro, which has been clearly shown; dthe virus or viral proteins are able to promote tumor formation in animals; an experimental model exists showing that nitrosamine carcinogens, together with HPV16 E6/E7 expression, induce oral cancer in transgenic mice4; dprophylactic HPV vaccination eliminates OSCC, but obtaining this “final proof” will require at least 20 years before declining trends in OSCC incidence will become evident. The major issue raised by Dr. Fleisher was not only the causality but the prevention of HPV infection by prophylactic HPV vaccination and health counseling to avoid oral sex. Several studies have shown the association between oral sex and oropharyngeal cancer.5 The transmission modes of HPV are not fully elucidated, but the evidence is sufficient that HPV also can transmit nonsexually. To shed more light on this topic, we will briefly refer to our studies in this long journey towards understanding HPV pathogenesis in oral mucosa. After showing the presence of HPV in oral lesions, we became more interested in asymptomatic oral HPV infections and their transmission, similar to the natural history studies on genital HPV infection. Our hypothesis in the early 1990s was that oral sex was the main transmission mode of oral HPV infection. However, we could not find such evidence in a cohort of 309 women followed up for their genital and oral HPV infection. Of the oral samples, 3.8 percent to 23 percent tested HPV positive, depending on the test.6 Only four women
Copyright © 2012 American Dental Association. All rights reserved.
COMMENTARY
had the same HPV genotypes in both oral and genital sites.6 Nine male partners had anogenital HPV infection, but all with different HPV types than those of their female partners in oral samples. Next, we became interested in the role of the mother in transmitting to her newborn. Among 98 infants born to 66 mothers, HPV was detected in 32 percent of the infants’ oral scrapings, of which 52 percent had the same HPV types as those in the genital sample of the mothers at delivery.7 We started a new study that also showed that vertically transmitted HPV was detectable from 2 days up to 3 years of age in 44 percent of the infants whose nasopharyngeal aspirate fluid tested HPV positive at birth. The overall concordance between HPV types found in the mother’s genital sample and
in her infant’s nasopharyngeal aspirate fluid was 69 percent.7 In the more recent Finnish HPV Family Study on HPV dynamics within a family, we failed to establish any significant association between oral sex and oral HPV infection during six years of follow-up, but persistent oral HPV infection in one spouse increased the risk of persistent oral HPV infection in the other spouse by 10-fold, indicating mouth-to-mouth transmission.8 We also showed that, at delivery, mother-newborn pairs had similar HPV genotype profiles (mother’s genital tract and newborn’s mouth), but this concordance disappeared in two months.9 Taken together, the mother might play a key role in transmitting HPV to her offspring. The significance of an early HPV infection is unknown, but theoretically the first HPV
JADA 143(5)
LETTERS
infection could determine the outcome of the other HPV infections during a lifetime. HPV vaccines might protect against HPV associated OSCC, but it will take several decades to prove it. As the evidence exists that HPV infection will be transmitted to at least some infants by their mothers, one could speculate that the most effective way to prevent HPVassociated OSCC (and also oropharyngeal cancer) is to vaccinate pregnant women or women before they become pregnant. Stina Syrjänen, DDS, PhD Professor and Chairman
Jaana Rautava, DDS, PhD Senior Researcher Department of Oral Pathology and Oral Radiology Institute of Dentistry Faculty of Medicine University of Turku Finland
http://jada.ada.org
Copyright © 2012 American Dental Association. All rights reserved.
May 2012 443
COMMENTARY
LETTERS
1. Syrjänen K, Syrjänen S, Lamberg M, Pyrhönen S, Nuutinen J. Morphological and immunohistochemical evidence suggesting human papillomavirus (HPV) involvement in oral squamous cell carcinogenesis. Int J Oral Surg 1983;12(6):418-424. 2. Rautava J, Syrjänen S. Human papillomavirus infections in the oral mucosa. JADA 2011;142(8):905-914. 3. Syrjänen S, Lodi G, von Bültzingslöwen I, et al. Human papillomaviruses in oral carcinoma and oral potentially malignant disorders: a systematic review. Oral Dis 2011;17 (suppl 1):58-72. 4. Strati K, Pitot HC, Lambert PF. Identification of biomarkers that distinguish human papillomavirus (HPV)-positive versus HPVnegative head and neck cancers in a mouse model. Proc Natl Acad Sci U S A 2006; 103(38):14152-14157. 5. Heck JE, Berthiller J, Vaccarella S, et al. Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Int J Epidemiol 2010;39(1):166-181. 6. Kellokoski JK, Syrjänen SM, Chang F, Yliskoski M, Syrjänen KJ. Southern blot hybridization and PCR in detection of oral human papillomavirus (HPV) infections in women with genital HPV infections. J Oral Pathol Med 1992;21(10):459-464. 7. Puranen M, Yliskoski M, Saarikoski S, Syrjänen KJ, Syrjänen SM. Exposure of an infant to cervical human papillomavirus infection of the mother is common. Am J Obstet Gynecol 1997;176(5):1039-1045. 8. Rintala M, Grénman S, Puranen M, Syrjänen S. Natural history of oral papillomavirus infections in spouses: a prospective Finnish HPV Family Study. J Clin Virol 2006;35(1):89-94. 9. Koskimaa HM, Waterboer T, Pawlita M, Grénman S, Syrjänen K, Syrjänen S. Human papillomavirus genotypes present in the oral mucosa of newborns and their concordance with maternal cervical human papillomavirus genotypes (published online ahead of print Dec. 5, 2011). J Pediatr.
In Dr. Mary Bush’s September JADA guest editorial, “Forensic Dentistry and Bitemark Analysis: Sound Science or Junk Science?” (JADA 2011;142[9]:997-999), the author raised serious questions about the appropriateness of bitemark analysis in legal proceedings, citing the 2009 National Academy of Sciences (NAS) report that took issue with facets of several historically accepted forensic identification methods.1 She failed to mention that the report also stated that “whether or not a forensic procedure is sufficient under the rules of evi-
dence governing criminal and civil litigation raises difficult legal issues that are outside the realm of scientific inquiry.”1(p190) Legal precedent is not determined by the guilt or innocence of the defendant; rather, the precedent is whether or not the court should consider the expert opinion proffered. An expert’s goal is the pursuit of truth, and mistaken accusations or incarcerations are a wrong that should be addressed. The forensic odontology community has taken and continues to take steps to ensure the validity of bitemark analysis. We have long espoused the belief that improved early recognition of bitemarks might lead to recovery of DNA. Many improvements in technology, in the understanding of the biology involved in injuries to human skin and in the application of scientific advances have been championed by the forensic odontology community. The American Board of Forensic Odontology (ABFO) has called for second opinions on casework and has worked diligently to provide guidelines and protocols for the proper analysis of bitemark evidence2 (as well as for human identification, disaster victim identification, abuse of persons and dental aging estimates). Bitemark injuries frequently occur during episodes of violence, impacting bitemark research. It is not possible to duplicate the circumstances surrounding bitemarks or the circumstances creating a specific bitemark at issue in a criminal case. Bitemark analysis depends upon the assumption that there is variation in each human dentition and that this variation may be recorded from a bite into human skin. Not every case is suitable for analysis; other cases never lead to the identifi-
444 JADA 143(5)
May 2012
BITEMARK ANALYSIS
http://jada.ada.org
cation or exclusion of a possible contributing biter. While we applaud research being conducted in Dr. Bush’s laboratory, that research is conducted on cadaveric materials, uses completed orthodontic dental models and is Procrustesbased, which does not take into account size differences between biters. Other researchers, some National Institute of Justice funded, have yet to publish their findings using experimental models differing from those of Dr. Bush. Research studying the individuality of the human dentition is significant and, when completed and incorporated into bitemark analysis, will likely change and improve how suspected biters’ teeth are evaluated. There has already been a shift in the paradigm of bitemark analysis, but that shift is not toward the concept that bitemark analysis is fatally flawed, but rather toward how to appropriately train, test and certify individuals in conducting analyses and in accrediting bodies responsible for expert certification. The real core of bitemark analysis issues is not with the practice of bitemark analysis, but with the practices of the analysts themselves. In fact, the NAS report recognized that bite marks in skin may (emphasis added) have limited validity due to innate features of the skin;1(p174) that individual practitioner skill bears on the results and analyses;1(p190) and champions the use of blind comparisons coupled with the use of a second expert.1(p175) The ABFO testified before the White House Subcommittee on Forensic Science in January 2011 and, pursuant to the subcommittee’s June 2011 request, furnished an annotated bibliography of 60-plus pages, including research conducted by
Copyright © 2012 American Dental Association. All rights reserved.
LETTERS
such as tobacco-use cessation and limiting alcohol use. Jennifer L. Cleveland, DDS, MPH Dental Officer and Epidemiologist
Michele L. Junger, DDS, MPH Dental Public Health Resident Division of Oral Health
Mona Saraiya, MD, MPH Medical Epidemiologist Division of Cancer Prevention and Control National Center for Chronic Disease Prevention and Health Promotion
Lauri E. Markowitz, MD
www.cdc.gov/mmwr/preview/mmwrhtml/ mm5920a4.htm. Accessed March 29, 2012. 4. Smith EM, Rubenstein LM, Haugen TH, Hamsikova E, Turek LP. Tobacco and alcohol use increases the risk of both HPV-associated and HPV-independent head and neck cancers. Cancer Causes Control 2010;21(9):1369-1378. 5. Fiore MC, Jaén CR, Baker TB, et al. Treating Tobacco Use and Dependence: 2008 Update—Clinical Practice Guideline. Rockville, Md.: U.S. Department of Health and Human Services, Public Health Service; 2008. www.surgeongeneral.gov/tobacco/ treating_tobacco_use08.pdf. Accessed March 29, 2012. 6. D’Souza G, Agrawal Y, Halpern J, Bodison S, Gillison ML. Oral sexual behaviors associated with prevalent oral human papillomavirus infection. J Infect Dis 2009;199(9): 1263-1269. 7. Kreimer AR, Villo A, Nyitray AG. The epidemiology of oral HPV infection among a multinational sample of men. Cancer Epidemiol Biomarkers and Prevention 2011; 20(1):172-182.
1. Glick M, Johnson N. Oral and oropharyngeal cancer: what are the next steps (editorial)? JADA 2011;142(8):892-894. 2. Centers for Disease Control and Prevention. FDA licensure of Quadrivalent Human Papillomavirus Vaccine (HPV4, Gardasil) for use in males and guidance from the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2010;59(20):630-632. www.cdc.gov/mmwr/ preview/mmwrhtml/mm5920a5.htm. Accessed March 29, 2012. 3. Centers for Disease Control and Prevention. FDA licensure of Bivalent Human Papillomavirus Vaccine (HPV2, Cervarix) for use in females and updated HPV vaccination recommendations from the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2010;59(20):626-629.
Response from Drs. Syrjanen and Rautava: We want to thank Dr. Fleisher for raising important questions concerning our article. Human papillomavirus (HPV) and oral squamous cell carcinoma (OSCC) has been a controversial issue since the first evidence was presented by us in 1983.1 As discussed, this is partly because of the wide variation in HPV detection rates.2 A recent meta-analysis of case-control studies confirmed that it is nearly fourfold more likely to find HPV DNA in oral cancer than in the control samples.3 However, to prove HPV as a cause of oral cancer, additional evidence is requested, summarized as “modified Koch’s postulates,” as follows: dviral infection precedes the development of cancer, which has not yet been formally shown, although the metaanalysis mentioned above gives the best evidence available to date to this notion3; dviral genome presents in tumor lesions or in tumor cells, which has been clearly confirmed; depidemiologic association between presence of the virus and development of cancer has not been shown because no ran-
442 JADA 143(5)
May 2012
Medical Epidemiologist
Eileen F. Dunne, MD, MPH Medical Epidemiologist Division of Sexually Transmitted Disease Prevention National Center for Hepatitis, HIV/AIDS, Sexually Transmitted Diseases, and Tuberculosis Prevention Centers for Disease Control and Prevention Atlanta
Joel B. Epstein, DMD, MSD, FRCD(C), FDS RCS(Edin) Director, Oral Medicine Adjunct Professor Division of Head and Neck Surgery City of Hope, Duarte, Calif. and Medical-Dental Staff Clinician Cedars-Sinai Medical Center Los Angeles
http://jada.ada.org
domized case-control or cohort studies have been published; dthe virus or viral proteins are able to transform cells in vitro, which has been clearly shown; dthe virus or viral proteins are able to promote tumor formation in animals; an experimental model exists showing that nitrosamine carcinogens, together with HPV16 E6/E7 expression, induce oral cancer in transgenic mice4; dprophylactic HPV vaccination eliminates OSCC, but obtaining this “final proof” will require at least 20 years before declining trends in OSCC incidence will become evident. The major issue raised by Dr. Fleisher was not only the causality but the prevention of HPV infection by prophylactic HPV vaccination and health counseling to avoid oral sex. Several studies have shown the association between oral sex and oropharyngeal cancer.5 The transmission modes of HPV are not fully elucidated, but the evidence is sufficient that HPV also can transmit nonsexually. To shed more light on this topic, we will briefly refer to our studies in this long journey towards understanding HPV pathogenesis in oral mucosa. After showing the presence of HPV in oral lesions, we became more interested in asymptomatic oral HPV infections and their transmission, similar to the natural history studies on genital HPV infection. Our hypothesis in the early 1990s was that oral sex was the main transmission mode of oral HPV infection. However, we could not find such evidence in a cohort of 309 women followed up for their genital and oral HPV infection. Of the oral samples, 3.8 percent to 23 percent tested HPV positive, depending on the test.6 Only four women
Copyright © 2012 American Dental Association. All rights reserved.
COMMENTARY
had the same HPV genotypes in both oral and genital sites.6 Nine male partners had anogenital HPV infection, but all with different HPV types than those of their female partners in oral samples. Next, we became interested in the role of the mother in transmitting to her newborn. Among 98 infants born to 66 mothers, HPV was detected in 32 percent of the infants’ oral scrapings, of which 52 percent had the same HPV types as those in the genital sample of the mothers at delivery.7 We started a new study that also showed that vertically transmitted HPV was detectable from 2 days up to 3 years of age in 44 percent of the infants whose nasopharyngeal aspirate fluid tested HPV positive at birth. The overall concordance between HPV types found in the mother’s genital sample and
in her infant’s nasopharyngeal aspirate fluid was 69 percent.7 In the more recent Finnish HPV Family Study on HPV dynamics within a family, we failed to establish any significant association between oral sex and oral HPV infection during six years of follow-up, but persistent oral HPV infection in one spouse increased the risk of persistent oral HPV infection in the other spouse by 10-fold, indicating mouth-to-mouth transmission.8 We also showed that, at delivery, mother-newborn pairs had similar HPV genotype profiles (mother’s genital tract and newborn’s mouth), but this concordance disappeared in two months.9 Taken together, the mother might play a key role in transmitting HPV to her offspring. The significance of an early HPV infection is unknown, but theoretically the first HPV
JADA 143(5)
LETTERS
infection could determine the outcome of the other HPV infections during a lifetime. HPV vaccines might protect against HPV associated OSCC, but it will take several decades to prove it. As the evidence exists that HPV infection will be transmitted to at least some infants by their mothers, one could speculate that the most effective way to prevent HPVassociated OSCC (and also oropharyngeal cancer) is to vaccinate pregnant women or women before they become pregnant. Stina Syrjänen, DDS, PhD Professor and Chairman
Jaana Rautava, DDS, PhD Senior Researcher Department of Oral Pathology and Oral Radiology Institute of Dentistry Faculty of Medicine University of Turku Finland
http://jada.ada.org
Copyright © 2012 American Dental Association. All rights reserved.
May 2012 443
COMMENTARY
LETTERS
1. Syrjänen K, Syrjänen S, Lamberg M, Pyrhönen S, Nuutinen J. Morphological and immunohistochemical evidence suggesting human papillomavirus (HPV) involvement in oral squamous cell carcinogenesis. Int J Oral Surg 1983;12(6):418-424. 2. Rautava J, Syrjänen S. Human papillomavirus infections in the oral mucosa. JADA 2011;142(8):905-914. 3. Syrjänen S, Lodi G, von Bültzingslöwen I, et al. Human papillomaviruses in oral carcinoma and oral potentially malignant disorders: a systematic review. Oral Dis 2011;17 (suppl 1):58-72. 4. Strati K, Pitot HC, Lambert PF. Identification of biomarkers that distinguish human papillomavirus (HPV)-positive versus HPVnegative head and neck cancers in a mouse model. Proc Natl Acad Sci U S A 2006; 103(38):14152-14157. 5. Heck JE, Berthiller J, Vaccarella S, et al. Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Int J Epidemiol 2010;39(1):166-181. 6. Kellokoski JK, Syrjänen SM, Chang F, Yliskoski M, Syrjänen KJ. Southern blot hybridization and PCR in detection of oral human papillomavirus (HPV) infections in women with genital HPV infections. J Oral Pathol Med 1992;21(10):459-464. 7. Puranen M, Yliskoski M, Saarikoski S, Syrjänen KJ, Syrjänen SM. Exposure of an infant to cervical human papillomavirus infection of the mother is common. Am J Obstet Gynecol 1997;176(5):1039-1045. 8. Rintala M, Grénman S, Puranen M, Syrjänen S. Natural history of oral papillomavirus infections in spouses: a prospective Finnish HPV Family Study. J Clin Virol 2006;35(1):89-94. 9. Koskimaa HM, Waterboer T, Pawlita M, Grénman S, Syrjänen K, Syrjänen S. Human papillomavirus genotypes present in the oral mucosa of newborns and their concordance with maternal cervical human papillomavirus genotypes (published online ahead of print Dec. 5, 2011). J Pediatr.
In Dr. Mary Bush’s September JADA guest editorial, “Forensic Dentistry and Bitemark Analysis: Sound Science or Junk Science?” (JADA 2011;142[9]:997-999), the author raised serious questions about the appropriateness of bitemark analysis in legal proceedings, citing the 2009 National Academy of Sciences (NAS) report that took issue with facets of several historically accepted forensic identification methods.1 She failed to mention that the report also stated that “whether or not a forensic procedure is sufficient under the rules of evi-
dence governing criminal and civil litigation raises difficult legal issues that are outside the realm of scientific inquiry.”1(p190) Legal precedent is not determined by the guilt or innocence of the defendant; rather, the precedent is whether or not the court should consider the expert opinion proffered. An expert’s goal is the pursuit of truth, and mistaken accusations or incarcerations are a wrong that should be addressed. The forensic odontology community has taken and continues to take steps to ensure the validity of bitemark analysis. We have long espoused the belief that improved early recognition of bitemarks might lead to recovery of DNA. Many improvements in technology, in the understanding of the biology involved in injuries to human skin and in the application of scientific advances have been championed by the forensic odontology community. The American Board of Forensic Odontology (ABFO) has called for second opinions on casework and has worked diligently to provide guidelines and protocols for the proper analysis of bitemark evidence2 (as well as for human identification, disaster victim identification, abuse of persons and dental aging estimates). Bitemark injuries frequently occur during episodes of violence, impacting bitemark research. It is not possible to duplicate the circumstances surrounding bitemarks or the circumstances creating a specific bitemark at issue in a criminal case. Bitemark analysis depends upon the assumption that there is variation in each human dentition and that this variation may be recorded from a bite into human skin. Not every case is suitable for analysis; other cases never lead to the identifi-
444 JADA 143(5)
May 2012
BITEMARK ANALYSIS
http://jada.ada.org
cation or exclusion of a possible contributing biter. While we applaud research being conducted in Dr. Bush’s laboratory, that research is conducted on cadaveric materials, uses completed orthodontic dental models and is Procrustesbased, which does not take into account size differences between biters. Other researchers, some National Institute of Justice funded, have yet to publish their findings using experimental models differing from those of Dr. Bush. Research studying the individuality of the human dentition is significant and, when completed and incorporated into bitemark analysis, will likely change and improve how suspected biters’ teeth are evaluated. There has already been a shift in the paradigm of bitemark analysis, but that shift is not toward the concept that bitemark analysis is fatally flawed, but rather toward how to appropriately train, test and certify individuals in conducting analyses and in accrediting bodies responsible for expert certification. The real core of bitemark analysis issues is not with the practice of bitemark analysis, but with the practices of the analysts themselves. In fact, the NAS report recognized that bite marks in skin may (emphasis added) have limited validity due to innate features of the skin;1(p174) that individual practitioner skill bears on the results and analyses;1(p190) and champions the use of blind comparisons coupled with the use of a second expert.1(p175) The ABFO testified before the White House Subcommittee on Forensic Science in January 2011 and, pursuant to the subcommittee’s June 2011 request, furnished an annotated bibliography of 60-plus pages, including research conducted by
Copyright © 2012 American Dental Association. All rights reserved.