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- Herausgeber: John Wiley & Sons
- Kategorie: Wissenschaft und neue Technologien
- Sprache: Englisch
An accessible, essential introduction to forensic odontology.
Written by a team of well-established, active practitioners in the field, Forensic Odontology is invaluable for those needing an introduction to the subject for the general dental practitioner who has an interest in forensic dentistry and is contemplating practicing in the field. It will also be useful as a reference during practice.
After a brief introduction the book covers dental anatomy and development, expert witness skills, mortuary practice, dental human identification, disaster victim identification, dental age assessment, bite marks, forensic photography and the role of the forensic odontologist in protection of the vulnerable person. Chapters outline accepted and recommended practices and refer to particular methodologies, presenting different schools of thought objectively.
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Seitenzahl: 544
Veröffentlichungsjahr: 2013
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Table of Contents
Title Page
Copyright
Dedication
List of contributors
Acknowledgements
Chapter 1: Brief introduction to forensic odontology
1.1 Introduction
1.2 Forensic odontology in the 21st century
1.3 Training and experience
1.4 How to use this book
1.5 References
Chapter 2: Development of the dentition
2.1 Early tooth development
2.2 Later tooth development
2.3 Dentinogenesis
2.4 Tooth root formation
2.5 Epithelial/mesenchymal interactions in tooth development
2.6 Amelogenesis
2.7 Biomineralisation of enamel
2.8 Further reading
Chapter 3: Acting as an expert witness
3.1 Introduction
3.2 The nature of expert evidence
3.3 The rules of court
3.4 The expert's duties
3.5 Report writing
3.6 Giving evidence at court
3.7 Ancillary topics
3.8 Things to avoid
3.9 A final thought
3.10 References
Chapter 4: Mortuary practice
4.1 Definitions of a mortuary
4.2 The Human Tissue Act and the Human Tissue Authority
4.3 Legal requirements for licence issue
4.4 Mortuary facilities
4.5 The Anatomical Pathology Technologist
4.6 The odontologist in the mortuary: Specialist resection techniques
4.7 Health and safety in the mortuary
4.8 References
Chapter 5: Dental human identification
5.1 Introduction
5.2 Comparative dental identification
5.3 Radiography in dental identification
5.4 Dental appliances in identification
5.5 Dental profiling
5.6 Teeth as a source of DNA
5.7 Conclusion
5.8 References
Chapter 6: Disaster victim identification
6.1 Introduction
6.2 Disaster management
6.3 DVI planning
6.4 DVI and the dentist
6.5 The dental DVI team structure
6.6 Documentation
6.7 Retrieval of dental records
6.8 Post-mortem dental examination
6.9 Ante-mortem dental records
6.10 Dental reconciliation
6.11 Equipment for the dental DVI team
6.12 Maintaining dental team morale
6.13 References
Chapter 7: Dental age assessment
7.1 The importance of knowing age
7.2 The chronological age
7.3 The dental age
7.4 Dentition as an age indicator
7.5 Age estimation methods in children and young adults
7.6 Age assessment after tooth development
7.7 Writing a dental age report
7.8 Final comments
7.9 References
Chapter 8: Bite marks—I
8.1 Introduction
8.2 Bite mark components
8.3 Nature of the injury
8.4 Bite mark incidence
8.5 Principles of bite mark analysis
8.6 Bite mark evidence recording
8.7 Bite mark analysis techniques
8.8 Feature-based analysis conclusions
8.9 Feature-based analysis report
8.10 Limitations of bite mark analysis
8.11 References
Chapter 9: Bite marks—II
9.1 Guidelines for bite mark analysis
9.2 Collection of evidence
9.3 Assessment of the suspected bite mark injury
9.4 Examination of the dentition of the suspected biter/biters
9.5 Bite mark comparisons
9.6 Bite mark reports and presentation of evidence to a court
9.7 References
Chapter 10: Forensic photography and imaging
10.1 Introduction
10.2 The photography of bite marks
10.3 Relevant equipment
10.4 Digital image file formats
10.5 Guidance for preparation of equipment for forensic photography
10.6 Photographing a bite mark
10.7 Photographing dentition
10.8 Image downloading and storage
10.9 Imaging modalities
10.10 Three-dimensional technology
10.11 Image enhancement and processing
10.12 References
Chapter 11: Role of the forensic odontologist in the protection of vulnerable people
11.1 Introduction
11.2 Bite marks and vulnerable people
11.3 Dental neglect in childhood
11.4 Legislative framework for child protection in the UK
11.5 Protection of the vulnerable adult
11.6 Record keeping
11.7 Summary chart
11.8 Further reading
11.9 References
Index
This edition first published 2014 © 2014 by John Wiley & Sons, Ltd
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Library of Congress Cataloging-in-Publication Data
Forensic odontology (Adams)
Forensic odontology : an essential guide / [edited by] Catherine Adams, Romina Carabott, and Sam Evans.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-119-96145-1 (cloth)
I. Adams, Catherine, 1960- editor of compilation. II. Carabott, Romina, editor of compilation. III. Evans, Sam, 1976- editor of compilation. IV. Title.
[DNLM: 1. Forensic Dentistry– methods. W 705]
RA1062
614′.18– dc23
2013024348
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
Sam Evans
To Emma, Jacob, Zach, Eli and Mabel
List of contributors
Acknowledgements
The editors would, first and foremost, like to thank all the contributors to this book. Their hard work and dedication have been instrumental in the completion of this joint effort.
Furthermore, without the tireless support from the editing team at Wiley this project would have ground to a halt long ago. Fiona, Nicky and Celia, we give you our thanks.
The editors would also like to thank all the colleagues who have supported us in this endeavour, with a special mention for the team at the Dental Illustration Unit, Cardiff University.
Lastly, the editors would like to give personal thanks to our loved ones who have supplied the endless patience and understanding we needed to finish this project.
Chapter 1
Brief introduction to forensic odontology
Romina Carabott
expertFORENSICS Ltd, Cardiff, UK
1.1 Introduction
According to Keiser Neilsen (1970; cited in Cameron and Sims, 1974), forensic odontology is:
that branch of dentistry which—in the interests of justice—deals with the proper handling and examination of dental evidence and with the proper evaluation and presentation of dental findings.
Forensic odontology, or dentistry, has been around for a long time: the identification of Lollia Paulina from her ‘distinctive’ teeth being as early as AD49, and the first use of bite mark evidence in court in a case of grave robbing in 1814.
The recent attention of the media on forensic ‘specialities’ featured in various fictional television series has seen an increased interest in this already fascinating subject. This heightened interest, however, has not always been for the right reasons. The use of dental identification in mass fatalities as the more efficient means of identification of severely decomposed bodies has attracted particular attention in natural disasters such as the Boxing Day tsunami in Thailand (2004), the Black Saturday bushfires in Australia (2009) and the Christchurch earthquake in New Zealand (2011). On the other hand, The Innocence Project (see references) has highlighted the ‘abuse’ and ‘misuse’ of bite mark analysis as reliable evidence in court; see also Bowers (2006), Pretty and Sweet (2010), Bush (2011) and Metcalfe et al. (2011).
To those involved in bite mark analysis research, this ‘attack’ on the validity of this identification science may not have come as a complete surprise (Clement and Blackwell, 2010; Pretty and Sweet, 2010). Bite mark evidence may be perceived by some in the investigative arena, who are not familiar with this area of forensic odontology, as a science akin to fingerprint analysis or DNA analysis. This is not the case, as was clearly highlighted in the report of the National Academy of Sciences (NAS) entitled Strengthening Forensic Science in the United States: A Path Forward (2009):
there also are important variations among the disciplines relying on expert interpretation. For example, there are more established protocols and available research for fingerprint analysis than for the analysis of bite marks. (p. 87)
Much forensic evidence—including, for example, bitemarks and forearm and tool mark identifications—is introduced in criminal trials without any meaningful scientific validation, determination of error rates, or reliability testing to explain the limits of the discipline. (p. 107)
The potential for bite mark evidence to be as useful as other forensic science disciplines may exist, but to date the very nature of the evidence renders sound and rigorous scientific research extremely difficult. Numerous publications have highlighted the lack of sound empirical evidence backing the two basic postulates of bite mark evidence and the paucity of rigorous research surrounding this discipline (Bowers, 2006; Pretty and Sweet, 2010; Bush, 2011). This is not to say that sound research has not been conducted over the years, but merely that more of such high-level research needs to come through. Until such a time when ‘the barriers to such encompassing and rigorous research to support bite mark evidence’ (Pretty, 2006) can be overcome, bite mark analysis needs to be applied to forensic case work with extreme caution.
A forensic odontologist's expertise in bite mark analysis lies in his/her ability to recognise the limitations of bite mark analysis for each individual case (Pretty, 2006). If such caution is applied, the credibility of bite mark analysis will not be irrevocable damage in the long term despite the wrongful convictions documented to date. With the progress of technology in leaps and bounds and ‘the willingness to utilise’ (Clement and Blackwell, 2010) such technology and science, there will still be a place for bite mark analysis in the investigators' arsenal.
Dental identification has attracted less media attention than bite mark analysis: the methodology is well understood and accepted, and its efficiency, cost-effectiveness and success have been witnessed on numerous occasions (Schuller-Götzburg and Suchanek, 2007; Bush and Miller, 2011; Hinchcliffe, 2011; Tengrove 2011); but that does not mean that it doesn't have challenges to contend with. Improvements in oral care—with an associated reduction of restorations available for comparison—highlight the importance of dental radiography which allows unique anatomical features to assist in establishing a dental identification. Chemical, biological, radiological and nuclear (CBRN) threats call for safe means of collecting dental evidence at the scene, such as cone-beam CT technology. Educating the members of the dental team in the advantages of dental identifications, ideally as early as undergraduate level, is required so as to continue to address the age-old problem of poor ante-mortem dental records which has always hindered the dental identification process. The advent of dental record keeping software addresses part of the problem but has been known to create other minor issues that must be kept in mind.
Mobilisation of individuals from areas of conflict into Europe has increased the requirement for a means to reliably assess the age of a living individual. Discussions are on-going, particularly in the UK, as to the reliability of dental age estimation of young adults and the ethical implications associated with exposing an individual to radiation for these purposes. In the author's view, the expertise of a forensic odontologist is not reflected in how well he/she mastered the age estimation techniques, but in his/her awareness of the limitations of these methods. Arguably, more important is the skill of explaining clearly to a judge and jury those same limitations and how they may apply to the particular case at hand. Interpreting the results and the statistical background of the methodology used in a way that is clear to the uninitiated is probably the main challenge; more so when various statistical approaches have been applied and then superseded over the years.
1.2 Forensic odontology in the 21st century
Forensic odontology has seen very few major developments over the last 20 years. Changes were mainly related to the assimilation of IT developments into this area of expertise. A very clear example is the improvement in bite mark analysis, previously relying on manual overlay production, while today it is often done with the aid of software such as Adobe Photoshop®.
Research and development in forensic odontology is hampered by two main problems:
Despite these difficulties over the last few years, through the dedication of those interested in this area and postgraduate student research, the application of forensic odontology is slowly acquiring a more robust backing from rigorous scientific research (Sheets et al., 2012, 2013; Bush et al., 2011). The application of medical devices, software and improved technology to address difficulties in forensic dentistry is seen as a move in the right direction.
The following are some examples of recent and current research:
Portable X-ray units
, developed largely with the veterinary services in mind, were brought to the attention of the international forensic dental community by the New Zealand DVI (Disaster Victim Identification) team during identification of the victims of the Boxing Day tsunami in Thailand. One of these units is now on the essential equipment list of the UK DVI team and, coupled with digital x-ray software, it eliminates the need for removing jaws for radiographic examination (both in isolated identifications as well as in mass fatality scenarios), when the only purpose for such removal of jaws is radiographic examination with traditional dental radiographic equipment.
Mobile multi-slice computed tomography
(MSCT) has been part of various research programmes into the application of virtual autopsies in multiple fatality scenarios where CBRN contamination is known or suspected. Concomitant current studies are also assessing whether a similar principle could be applied to dental identification in such scenarios. Cone-beam CT (CBCT) technology provides superior quality dental detail to MSCT and, if applicable, may have the potential to provide post-mortem dental information without the need for direct examination of contaminated bodies.
Three-dimensional imaging
for patterned injuries (bite marks) is being researched in various facilities around the world. If developed adequately it could not only eliminate the photographic distortion that affects bite mark analysis but could also increase the versatility of analytical methods and the presentation of evidence in court (Evans
et al
., 2010; Blackwell
et al
., 2007; Thali
et al
., 2003).
Computer-generated skin/human body modelling
could resolve the ethical issues with bite mark analysis, providing a means of studying the effects of force, friction, movement, time and tooth features in relation to the reaction of living human tissue, skin being such a notoriously poor impression material (Stam
et al
., 2010, 2012; Whittle
et al
., 2008).
However, without the investment by academic departments, funding bodies and research councils, the advance of forensic dentistry will continue to be at a very slow rate.
1.3 Training and experience
There is to date no universally accepted pathway for training to become a forensic odontologist other than the requirement of obtaining a degree in dental surgery and being registered with the national regulatory body to practice dentistry. Different countries have different courses or training pathways, so if someone is interested in getting involved in the analysis of forensic dental evidence he/she should refer to the national organisation for forensic odontology. Table 1.1 lists some of these associations with their respective website (where available). This is not a comprehensive list: new associations/groups will continue to be set up as the knowledge and awareness of the subject spreads.
Table 1.1 Forensic odontology/dentistry organisations
American Board of Forensic Odontology
www.abfo.org
American Society of Forensic Odontology
www.asfo.org
Australian Society of Forensic Odontology
www.ausfo.com.au
Austrian Society of Forensic Medicine (ÖGGM)
www.oeggm.com
British Association for Forensic Odontology
www.bafo.org.uk
Canadian Society of Forensic Science
www.csfs.ca
Croatian Association of Forensic Stomatologists
Danish Society of Forensic Odontology(Dansk RetsOdontologisk Forening)
www.retsodont.dk
Finnish Association of Forensic Odontology
www.apollonia.fi
Flemish Association of Dental Experts
French Association of Dental Identification(Association Francaise d'Identification Odontologique)
www.adf.asso.fr
German Academy of Forensic Odontostomatology(Arbeitskreis für Forensische Odonto-Stomatologie)
www.akfos.com
Icelandic Society of Forensic Odontology
Indian Association of Forensic Odontology
www.theiafo.org
International Association for Forensic Odonto-Stomatology
www.iofos.eu
Israel National Police Volunteer Dentists Unit
Italy—Forensic Odontology Project(ProOF—Progetto Odontologia Forense)
www.proofweb.eu
Netherlands(Forensisch Medisch Genootschap)
www.forgen.nl
New Zealand Society of Forensic Odontology
www.nzsfo.org.nz
Norwegian Society of Forensic Odontology
Polish Society of Forensic Odontology
www.ptos.pl
South African Society for Forensic Odonto-Stomatology
Switzerland(Forensische Zahnärtze der Schweiz)
www.sso.ch
The International Organisation of Forensic Odonto-Stomatology (IOFOS; www.iofos.eu) aims to liaise between forensic odontology societies on a global basis and should be an early port of call if someone is unable to identify a national association for forensic odontology in their own country.
The national associations will be able to provide advice on the accepted pathway by which a dentist may gain experience as a forensic odontologist/dentist and practise within the legal framework of the country in question following recommended guidelines of good practice. Joining these associations also allows the interested dentist to learn more about the day-to-day experience of being a forensic dentist from those who have been practising for some years. It may come as a surprise to some, how unglamorous the reality is in comparison to the life of forensic specialists portrayed in the various crime dramas aired on the media.
A handful of structured postgraduate degrees exist and have for some time been the entry point for those who express an interest in training in this field. Few as they are, these courses (ranging from Diploma to Masters levels) are becoming even rarer as some of them become victims to lack of funding.
It is the author's and editors' view that, while a structured postgraduate course is an excellent start, it is important for those who qualify to then spend some time shadowing an experienced forensic dentist in the field, ideally on a mentoring scheme. No course, no matter how in-depth and how practical it is, can recreate a case in the field, particularly when it comes to bite mark analysis. The latter requires experience not only in handling and collecting the evidence but also in the analysis itself, due to the variety of scenarios and circumstances that makes each case unique.
As an example, the British Association for Forensic Odontology (BAFO; www.bafo.org.uk) has now established a mentoring scheme whereby dentists who have qualified from a postgraduate degree in forensic odontology and who wish to practise in the field are assigned a mentor in their geographical area. The mentor is someone with some years of experience in the field and, together with the mentee, he/she puts together a personal development plan. This plan will include a period of observation by the mentee and eventually a period of being under observation during actual cases until both mentor and mentee feel confident that the mentee can practise independently.
The above applies to the practice of forensic odontology in the UK. Different recommendations/pathways will apply in other countries.
1.4 How to use this book
The intention of this book is, in the first instance, to act as an introduction to forensic odontology for the general dental practitioner who has an interest in forensic dentistry and is contemplating practising in the field. It can also be utilised as a companion and reference during practice.
Most chapters will outline accepted and recommended practices and refer to particular methodologies. Where different schools of thought exist, they will be outlined objectively. The reader is advised to use the book as a starting point rather than the one and only source of information, as well as a reference to guidelines of good practice.
It is beyond the scope of the book to cover in full detail areas such as basic dental science, the law as it pertains to practising as an expert witness, mortuary practice, and protection of the vulnerable person. Dedicated specialist texts are available that expand on these subjects.
As noted previously, the editors believe that a book or a series of lectures alone, no matter how comprehensive, are not sufficient to qualify a person to become a forensic odontologist. Such media will provide the information, but the true acquisition of knowledge in the field comes with practical mock scenarios and observation/practice on real cases under the mentorship of experienced practitioners.
The contributors to this book are all experts in their respective fields and understand the needs of the forensic odontologist and how the respective fields interact in practice.
Most of the chapters can stand alone so that the book doesn't have to be read sequentially. However, the ordering of the chapters follows what the editors believe is the correct approach to building up one's knowledge of forensic odontology.
We hope you can enjoy discovering forensic odontology and that this book will encourage you to research more about this field. We welcome any feedback or comments.
1.5 References
Blackwell S. A., Taylor R. V., Gordon I., Ogleby C. L., Tanijiri T., Yoshino M., Donald M. R. and Clement J. G. (2007) 3-D imaging and quantitative comparison of human dentitions and simulated bite marks, International Journal of Legal Medicine121: 9–17.
Bowers C. M. (2006) Problem-based analysis of bitemark misidentifications: the role of DNA, Forensic Science International159S: S104–S109. ScienceDirect [Online]. Available at: www.sciencedirect.com (accessed 20 March 2013).
Bush M. A. (2011) Forensic dentistry and bitemark analysis: sound science or junk science?, Journal of the American Dental Association142(9): 997–999. Highwire Press American Dental Association [Online]. Available at: http://jada.ada.org (accessed 20 March 2013).
Bush M. A., Bush P. J. and Sheets H. D. (2011) A study of multiple bitemarks inflicted in human skin by a single dentition using geometric morphometric analysis, Forensic Science International211(1–3): 1–8. ScienceDirect [Online]. Available at: www.sciencedirect.com (accessed 25 March 2013).
Bush M. and Miller R. (2011) The crash of Colgan Air flight 3407: advanced techniques in victim identification, Journal of the American Dental Association142(12): 1352–1356. Highwire Press American Dental Association [Online]. Available at: http://jada.ada.org (accessed 10 September 2012).
Cameron J. M. and Sims B. G. (1974) Forensic Dentistry. Edinburgh:Churchill Livingstone.
Clement J. G. and Blackwell S. A. (2010) Is current bite mark analysis a misnomer?, Forensic Science International201: 33–37. ScienceDirect [Online]. Available at: www.sciencedirect.com (accessed 20 March 2013).
Evans S., Jones C. and Plassmann P. (2010) 3D imaging in forensic odontology, Journal of Visual Communication in Medicine33(2): 63–68.
Hinchliffe J. (2011) Forensic odontology. Part 2: Major disasters, British Dental Journal210(6): 269–274.
Metcalfe R. D., Lee G., Gould L. A. and Stickels J. (2011) Bite this! The role of bite mark analyses in wrongful convictions, Southwest Journal of Criminal Justice7(1): 47–64.[Online]. Available at: www.forensic-dentistry.info/wp/wp-content/uploads/2011/07/Metcalf-et-al.1.pdf (accessed 25 March 2013). National Academy of Science (2009) Strengthening Forensic Science in the United States: A Path Forward. [Online]. Available at: www.nap.edu/catalog/12589.html (accessed 20 March 2013).
Pretty I. A. (2006) The barriers to achieving an evidence base for bitemark analysis. Forensic Science International159(suppl 1): S110–S120 (review).
Pretty I. A. and Sweet D. (2010) A paradigm shift in the analysis of bitemarks, Forensic Science International201: 38–44. ScienceDirect [Online]. Available at: www.sciencedirect.com (accessed 20 March 2013).
Schuller-Götzburg P. and Suchanek J. (2007) Forensic odontologists successfully identify tsunami victims in Phuket, Thailand, Forensic Science International171(2–3): 204-207. ScienceDirect [Online]. Available at: www.sciencedirect.com (accessed 20 March 2013).
Sheets H. D., Bush P. J. and Bush M. A. (2012) Bitemarks: distortion and covariation of the maxillary and mandibular dentition as impressed in human skin, Forensic Science International223(1–3): 202–207. ScienceDirect [Online]. Available at: www.sciencedirect.com (accessed 25 March 2013).
Sheets H. D., Bush P. J. and Bush M. A. (2013) Patterns of variation and match rates of the anterior biting dentition: characteristics of a database of 3D-scanned dentitions, Journal of Forensic Sciences58(1): 60–68. Swetswise [Online]. Available at: www.swetswise.com (accessed 25 March 2013).
Stam B., van Gemert M., van Leeuwen T. and Aalders M. (2010) 3D finite compartment modelling of formation and healing of bruises may identify methods for age determination of bruises, Medical and Biological Engineering and Computing48(9): 911–921.
Stam B., Gemert M., Leeuwen T. and Aalders M. (2012) How the blood pool properties at onset affect the temporal behaviour of simulated bruises, Medical and Biological Engineering and Computing50(2): 165–171.
Tengrove H. (2011) Operation earthquake 2011: Christchurch earthquake disaster victim identification, Journal of Forensic Odontostomatology29(2): 1–7. Journal of Forensic Odontostomatology Online [Online]. Available at: www.iofos.eu/JFOSOnline2.html (accessed 20 March 2013).
Thali M. J., Braun M., Markwalder Th. H., Brüschweiler W., Zollinger U., Malik Naseem J., Yen K. and Dirnhofer R. (2003) Bite mark documentation and analysis: the forensic 3D/CAD supported photogrammetry approach, Forensic Science International135: 115–121. The Innocence Project (undated: accessed 6 June 2013): http://innocenceproject.org/Content/Cases_Where_DNA_Revealed_that_Bite_Mark_Analysis_Led_to_Wrongful_Arrests_and_Convictions.php
Whittle K., Kieser J., Ichim I., Swain M., Waddell N., Livingstone V. and Taylor M. (2008) The biomechanical modelling of non-ballistic skin wounding: blunt-force injury Forensic Science, Medicine, and Pathology4(1): 33–39.
Chapter 2
Development of the dentition
Alastair J. Sloan
School of Dentistry, Cardiff University, UK
The process of tooth development—or odontogenesis—is a complex series of reciprocal cellular interactions, by which teeth form from epithelial and mesenchymal cells in the stomatodeum. Enamel, dentine, cementum and the periodontium must all develop during appropriate stages of embryonic development. Primary teeth begin to form between the sixth and eighth weeks of intrauterine (i.u.) life, and permanent teeth begin to form in the twentieth week. If teeth do not start to develop around those times, it is likely that they will not develop at all and be missing.
2.1 Early tooth development
The stomatodeum is lined by a primitive epithelium which is two or three cells in thickness. Beneath this is embryonic connective tissue, the ectomesenchyme (Figure 2.1). The first sign of tooth development within the stomatodeum is a thickening of the epithelium and this thickening is called the primary epithelial band. It forms at around 6 weeks of i.u. life and indicates the position of the future dental arches. The primary epithelial band rapidly divides into two structures, the dental lamina and the vestibular lamina. The latter ultimately gives rise to the vestibule/sulcus while the former gives rise the to the tooth germs. At 6 weeks there is no vestibule/sulcus between cheek and tooth-bearing area. The vestibule forms from proliferation of vestibular lamina into the ectomesenchyme. The vestibular lamina cells rapidly enlarge, then degenerate leaving a cleft which becomes the vestibule.
Figure 2.1 (a) Stomatodeum with primary epithelial band (arrow). MP, maxillary process; T, tongue; MA, mandibular arch. (b) Primary epithelial band at high magnification
The dental lamina is the structure that gives rise to the tooth germs, and proliferation of the dental lamina at 6–7 weeks i.u. determines the positions of future deciduous teeth with a series of 20 epithelial ingrowths into ectomesenchyme (10 in each development jaw). This first incursion of the epithelial dental lamina into the mesenchyme leads to a bud of cells at the distal aspect of the dental lamina and is called the bud stage of tooth development (Figure 2.2). Each bud is separated from the ectomesenchyme by a basement membrane. There is little change in shape or function of the epithelial cells at this time. The supporting ectomesenchymal cells congregate around the bud, forming a cluster of cells which are closely packed beneath and around the epithelial bud, which is the initiation of the condensation of the ectomesenchyme. The remaining ectomesenchymal cells are arranged with less regular order.
Figure 2.2 Bud stage of tooth development (arrow). The bud is formed from the invading epithelium and condensation of the surrounding ectomesenchymal cells
As tooth development progresses, two key processes become essential to development. The first is morpho-differentiation, which is the determination of the shape of the crown of the tooth through the shape of the amelodentinal junction of the forming tooth. The second process is histo-differentiation, where cells of the developing tooth differentiate (specialise) into morphologically and functionally distinct groups of cells responsible for secretion of various dental tissues. Control and regulation of this differentiation is through specific and reciprocal cellular interactions between the epithelial/mesenchymal compartments.
As the epithelial bud continues to proliferate into the ectomesenchyme, the first signs of an arrangement of cells in the tooth bud appear in the cap stage. A small group of ectomesenchymal cells stops producing extracellular substances and do not separate from each other, which results in an aggregation or condensation of these cells immediately adjacent to the epithelial bud. This is the developing dental papilla. At this point, the tooth bud grows around the ectomesenchymal aggregation, taking on the appearance of a cap, and becomes the enamel (or dental) organ. A condensation of ectomesenchymal cells called the dental follicle surrounds the enamel organ and limits the dental papilla (Figure 2.3). The enamel organ is responsible for the synthesis and secretion of enamel, the dental papilla will lead to the formation of the dentine and pulp, and the dental follicle will produce the supporting structures of a tooth. This explains why enamel is epithelial in origin whereas dentine, pulp and periodontal tissues are mesenchymally derived.
Figure 2.3 Cap stage of tooth development where the three components of the tooth germ can be observed. EO, enamel organ; DP, dental papillae; DF, dental follicle
As tooth development proceeds there is a distinct histo- and morpho-differentation of the enamel organ as it prepares for secretory function, along with an increase in size of the tooth germ. This change signifies the transition to the early bell stage. The enamel organ takes on a bell shape during this stage with continued cell proliferation, and histo-differentiation of four distinct cell layers within the enamel organ can be observed (Figure 2.4).
Figure 2.4 Bell stage of tooth development where the four cell layers of the enamel organ can be observed. SR, stellate reticulum; SI, stratum intermedium; arrow, outer enamel epithelium; arrowhead, inner enamel epithelium
A single layer of cubiodal cells at the periphery of the enamel organ limit its size and are known as the outer enamel epithelium. Conversely, the single cell layer adjacent to the dental papilla is known as inner enamel epithelium and it is these cells that will differentiate into ameloblasts and give rise to enamel synthesis and secretion. Where these cells of the inner and outer enamel epithelium meet is termed the cervical loop. The majority of the cells that are situated between the outer and inner enamel epithelium are termed the stellate reticulum. These cells secrete hydrophilic glycosaminoglycans which increase the extracellular space and the cells interconnect through desmosomes giving them a stellate or star-shaped appearance. A layer two or three cells thick lying next to the inner enamel epithelium, and having a flattened shape, is termed the stratum intermedium. In summary, the layers of the enamel organ in order of innermost to outermost consist of inner enamel epithelium, stratum intermedium, stellate reticulum and outer enamel epithelium.
During this stage of development, as it progresses from cap stage to early bell stage, a localised thickening of cells at the inner enamel epithelium around the cusp tip appears. This is known as the enamel knot and is a signalling centre of the tooth that provides positional information for tooth morphogenesis and regulates the growth of tooth cusps. The enamel knot produces a range of molecular signals from all the major growth factor families, including fibroblast growth factors (FGF), bone morphogenetic proteins (BMP), Hedgehog (Hh) and Wnt signals. These molecular signals direct the growth of the surrounding epithelium and mesenchyme and have putative roles in signalling and regulation of crown development. The enamel knot is transitory and the primary enamel knot is removed by apoptosis. Later, secondary enamel knots may appear that regulate the formation of the future cusps of the teeth.
2.2 Later tooth development
As tooth development progresses from the early bell stage to a late bell stage of development, epithelial/mesenchymal interactions signal further histo-differentiation of the four cell layers of the enamel organ in preparation for amelogenesis. Cell appearance in the enamel organ is directly related to function. The cells of the outer enamel epithelium are cuboidal with a high nuclear:cytoplasm ratio. These cells have a non-secretory protective role and will eventually become part of the dentogingival junction. The stellate reticulum cells sit in a substantial jelly-like extracellular matrix which protects the interior of a tooth germ. The cells of the inner enamel epithelium have a low columnar appearance with a central nucleus and few organelles. These cells are at a preparatory stage of becoming secretory, the ameloblast.
The inner enamel epithelial cells are separated from the ectomesenchymal dental papillae by the dental basement membrane. This structure mediates interactions between the epithelial and mesenchymal compartments of the tooth germ during development and odontoblast differentiation prior to dentine secretion. At this time, the dental papillae contains undifferentiated ectomesenchymal cells with relatively small amounts of extracellular matrix (apart from a few fine collagen fibrils) and these cells are not yet specialised for secretory function.
The late bell stage is also known as the crown stage of tooth development and further cellular changes occur at this time. In all prior stages of tooth development, all of the inner enamel epithelium cells were proliferating to contribute to the increase of the overall size of the tooth germ. However, during the crown stage, cell proliferation stops at the location corresponding to the sites of the future cusps of the teeth. At the same time, the inner enamel epithelial cells change in shape from cuboidal to short columnar cells with nuclei polarised to the end of the cell away from the basement membrane.
The adjacent layer of cells on the periphery of the dental papilla increases in size, the cells become columnar and their nuclei polarise away from the basement membrane as they differentiate into odontoblasts. These changes to the inner enamel epithelium and the differentiation of odontoblasts begin at the site of the future cusp tips and the odontoblasts secrete an organic collagen-rich matrix called pre-dentine, towards the basement membrane. As the odontoblasts secrete pre-dentine, they retreat and migrate toward the centre of the dental papilla. Cytoplasmic extensions are left behind as the odontoblasts move inward, creating a unique, tubular microscopic appearance of dentine as pre-dentine is secreted around these extensions.
After dentine formation begins, the dental basement membrane breaks down and the short columnar cells of the inner enamel epithelium come into contact with the pre-dentine, terminally differentiate into ameloblasts and begin to secrete an organic-rich matrix against the dentine. This matrix is partially mineralised and will mature to become the enamel. Whereas dentine formation proceeds in a pulpal direction, enamel formation moves outwards, adding new material to the outer surface of the developing tooth.
During this stage of tooth development, the tooth germ loses attachment to oral epithelium as it becomes encased in bone of developing jaws. The dental lamina begins to disintegrate into discrete islands of cells known as the Glands of Serres. Most of these degenerate but some remain quiescent in jaw bone; if stimulated later in life they may form odontogenic cysts known as ‘odontogenic keratocysts’. The vascular supply enters dental papilla during the cap stage of development and increases during the bell stage during hard tissue formation. The vasculature enters the dental papilla around sites of future root formation. The pioneer nerve fibres approach the developing tooth germ during the bud/cap stage but do not penetrate dental papilla until dentine formation begins.
Formation of the permanent dentition arises from a proliferation and extension of the dental lamina. The permanent incisor, canine and premolar germs arise from proliferation on the lingual aspect of the dental lamina next to their deciduous predecessors. The permanent molars have no deciduous predecessors and develop from backward extension of the dental lamina which gives off epithelial ingrowths giving rise to the first, second and third permanent molars.
2.3 Dentinogenesis
The secretion of dentine matrix begins at 17–18 weeks i.u., corresponding to the late bell stage (crown stage) of tooth development. Odontoblast differentiation begins at the future cusp tip, spreading apically down a gradient of differentiation down the cuspal slopes. Dentine formation, or secretion of a dentine matrix, starts immediately following odontoblast differentiation. Odontoblast differentiation can be characterised by a distinct change in cell phenotype and morphology. The ectomesenchymal cells of dental papilla have a high nucleus to cytoplasm ratio, little rough endoplasmic reticulum and few mitochondria, so they have a low synthetic/secretory activity. As these cells differentiate into odontoblasts, they become cells with a low nuclear to cytoplasm ratio and have increased rough endoplasmic reticulum, golgi and mitochondria and develop a high synthetic/secretory capacity.
The cells of the inner enamel epithelium are critical to the formation of dentine and odontoblast differentiation through molecular signalling. The basement mediates presentation of these molecules, which include the growth factors fibroblast growth factor and bone morphogenetic protein. As odontoblasts differentiate and secrete pre-dentine, the basement membrane breaks down and the cells of the inner enamel epithelium become exposed to pre-dentine which signals ameloblast differentiation. As well as receiving the chemical/molecular signals, the dental papilla cells must also be competent to respond to that signal for differentiation to occur. Competency is achieved by the cells undergoing the requisite number of cell cycles; and after the final cell division and cell alignment at the periphery of the dental papilla, the cell nearest the inner enamel epithelium receives these molecular signals from the enamel organ and differentiates into an odontoblast (Figure 2.5). The other daughter cell remains undifferentiated and exists within the developed pulp as a sub-odontoblast in the cell-rich layer. Odontoblasts are post-mitotic and they undergo no further cell division. Once differentiated, they begin to secrete pre-dentine which is an unmineralised dentine matrix.
Figure 2.5 Odontoblast differentiation is controlled by reciprocal epithelium/mesenchymal interactions mediated by the dental basement membrane. Signals are passed between the inner enamel epithelium (IEE) to the cells at the periphery of the dental papillae (DP) though the basement membrane (BM). After one final cell division, the daughter cell nearest the basement membrane receives the signal which mediates differentiation into an odontoblast cell, while the other daughter cell remains undifferentiated
The first formed dentine is termed mantle dentine and is approximately 0.15 mm thick. This matrix is synthesised and secreted from both newly differentiated odontoblasts and existing dental papilla cells (the rest of the dentine matrix is secreted from odontoblasts alone). Mineralisation of this mantle dentine is via matrix vesicles. After mantle dentine formation, odontoblasts continue to secrete pre-dentine which mineralises to dentine, and this, secreted throughout the remainder of tooth development, is termed primary dentine. The odontoblasts always secrete a layer of pre-dentine which mineralises to dentine and as they secrete pre-dentine, the cells retreat pulpally. As the cells retreat, they leave a single cytoplasmic process within the matrix which allows the odontoblast to communicate with the deeper layers of matrix. This process also creates the tubular structure of dentine which runs throughout the tissue. These tubules follow an S-shaped course in coronal dentine, but a straighter course in radicular dentine.
There are two levels of matrix secretion from the odontoblast and it is this which contributes to the unique structure of dentine. The main secretion of structural components (collagen, proteoglycans) into pre-dentine comes from the cell body of the odontoblast. The pre-dentine matrix is secreted around and between the extending odontoblast process and this leads to formation of tubules within the matrix, with each tubule containing an odontoblast process. This creates the tubular structure of dentine and this dentine matrix secreted from the odontoblast cell body is termed intertubular dentine. A second level of secretion of a dentine matrix, rich in tissue-specific matrix components at the mineralisation front, is within each dentinal tubule. This is termed intratubular or peritubular dentine and is found immediately surrounding the inside of the dentinal tubule. It is highly mineralised with little collagen. It is thought that secretion of peritubular dentine is from the odontoblast process.
Dentine forms rhythmically during development, with the odontoblast alternating between periods of pre-dentine secretion and quiescence. As a result, incremental lines can be observed and these correspond to a daily rate of secretion of pre-dentine of 4 m per day. At the boundary between these daily increments, minute changes in collagen fibre orientation can be noted. In addition to these daily incremental lines, a 5-day pattern of secretion can be observed and these incremental lines run at 90 degrees to the dentinal tubules and highlight the normal rhythmic and linear pattern of dentine secretion. These incremental lines are known as the Lines of Von Ebner and are approximately 20 m apart.
2.4 Tooth root formation
Roots are incomplete at eruption and root development is completed approximately 12 months post eruption for deciduous teeth and 2–3 years post eruption for the permanent dentition.
The root is formed primarily of dentine but is lined with cementum. For root formation to begin, epithelial tissue is required to map out the shape of the tooth and initiate and mediate root odontoblast differentiation and subsequent dentine secretion. The epithelium responsible for this is known as Hertwig's Epithelial Root Sheath (HERS) and is formed from a downward growth of the cervical loop. The HERS is bilaminar, consisting of cells from both the inner and outer enamel epithelium, and it grows as a collar enclosing the future root. The inner cells of the HERS do not differentiate into ameloblasts, but they are responsible for inducing cells on the periphery of the dental papilla, adjacent to the HERS to differentiate into odontoblasts for root dentine secretion. As in the crown, a gradient of root odontoblast differentiation and root dentine secretion can be observed from crown to root apex. The HERS fragments once root dentine secretion begins and exposes the root surface to the ectomesenchymal cells of the dental follicle. This stimulates follicular cells adjacent to the root dentine to differentiation into cementoblasts which are responsible for cementogenesis and secretion of cementum. The HERS fragments lie adjacent to the root as cell clusters and are generally quiescent and functionless. These clusters are known as the Cell Rests of Malassez and, although quiescent, can be stimulated to proliferate during periods of inflammation (e.g. pulpitis) and give rise to dental (radicular) cysts.
Two types of cementum are formed: cellular and acellular. As cementoblasts differentiate from the follicular cells they begin to secrete collagen fibrils and non-collagenous proteins (e.g. bone sialoprotien, osteocalcin) along and at right-angles to the root surface before migrating away from the developing root. As the cementoblasts migrate, more collagen is deposited. This is acellular cementum and is the first formed cementum. The matrix secreted by the cementoblasts subsequently mineralises. During mineralisation the cementoblasts move away from the cementum, and the collagen fibres left along the surface of the root eventually join the forming periodontal ligament fibres. Cellular cementum is formed once the majority of the tooth development is complete and once the tooth is present in the occlusion. Cellular cementum is formed around the collagen fibre bundles and the cementoblasts become entrapped within the matrix they produce. These cells trapped within the cementum are termed cementocytes.
The origin of cementoblasts is thought to be different for acellular and cellular cementum. Current thinking is that cementoblasts responsible for acellular cementum arise from the ectomesenchymal cells of the dental follicle adjacent to the developing root dentine, whereas cementoblasts responsible for the synthesis and secretion of cellular cementum migrate from the adjacent area of bone. Interestingly, cellular cementum is not commonly found in single-rooted teeth; however, in premolars and molars it is found only in the part of the root closest to the apex and in interradicular areas between multiple roots.
It is also thought that the inner cells of the HERS have a very brief secretory phase prior to it fragmenting. This results in the secretion of a thin hyaline layer of tissue containing enamel-like proteins. It is most prominent in the apical area of molars and premolars and less obvious in incisors and deciduous teeth.
Differential proliferation of the HERS in multi-rooted teeth causes the division of the root into two or three roots, as local proliferation causes invaginations of the HERS. Ingrowth of the rooth sheath towards the end of root development is responsible for apical closure of the root.
2.5 Epithelial/mesenchymal interactions in tooth development
Sequential and reciprocal signalling between the epithelial (enamel organ) and mesenchymal (dental papilla) compartments of the tooth germ regulates the formation of the complex shape of individual teeth. Signalling molecules of different families mediate cell communication during tooth development. The majority of these belong to the transforming growth factor beta (TGFβ), fibroblast growth factor (FGF), Hedgehog and Wnt families. These signals generally regulate interactions between the enamel organ and dental papilla, but they may also mediate cell-to-cell communication within each tissue compartment. The genes regulated by these different signals include transcription factors and those encoding for cell surface receptors (on cells in either the enamel organ or dental papilla) that regulate the competence of those cells to respond to the next signals. They also regulate the ability of the cells to respond to new signals that act reciprocally, which maintains communication between the enamel organ and dental papilla.
The appearance of transient signalling centres in the enamel organ during tooth development is crucial to maintaining these epithelial/mesenchymal interactions and thus allowing tooth development to proceed. The first of these centres appears during the bud stage and then again when the enamel knot(s) appear. They may express many different signalling molecules, including sonic hedgehog (Shh), BMPs, FGFs and Wnts, and regulate coronal development and the initiation of the secondary enamel knot(s) at the sites of the folding of the inner enamel epithelium leading to cusp formation.
One of the first signalling events in tooth development addresses the question of how a tooth knows to become a tooth. Tissue recombination studies have shown that the jaw epithelium controls events which commit the neural crest cells of the ectomesenchyme to become teeth and the BMPs and FGFs regulate this process. It is the epithelium which induces cell competence in the mesenchyme to drive subsequent tooth development. Further tissue recombination studies using a mix of dental epithelium or dental mesenchyme and skin epithelium or skin mesenchyme confirmed this, as combining dental epithelium with skin mesenchyme gave rise to a skin-like tissue, whereas recombining skin epithelium with dental mesenchyme led to progression of dental tissue. The growth factors BMPs and FGFs induce the expression of several transcription factors in the developing dental papilla, many of which are essential for tooth development to progress. These include the transcription factors Msx1 and Pax9.
The first epithelial signals induce in the mesenchyme the expression of reciprocal signal molecules (FGF and BMP4), which act back on the epithelium regulating the formation of the primary epithelial band. Further signals then regulate formation of the bud stage and condensation of the ectomesenchymal cells. These cells of the ectomesenchyme maintain the expression of transcription factors (e.g. Msx1) which had been earlier induced by signalling from the jaw epithelium, and this upregulates the expression of new genes (such as the transcription factor Runx2 and the signalling molecule FGF3), which then regulates progression from the bud to cap stage. At the same time, BMP4 expression in the ectomesenchyme is required for the formation of the enamel knot. The enamel knot cells express many signalling molecules and these influence both epithelial and ectomesenchymal cells. Reciprocal interactions between the mesenchyme and epithelium maintain the enamel knot and mediate the formation of the four cell layers within the developing enamel organ. SHH is another important signalling molecule as its secretion from the enamel knot influences growth of the cervical loops. It also regulates crown patterning (crown shape) by initiating formation of the secondary enamel knots which determine the sites where the inner enamel epithelium folds (due to differential cell proliferation) and cusp development starts.
To understand how we get teeth of different shapes in the correct position in the dental arch (patterning of the dentition), two theories have been proposed:
The
field model
proposes that local factors responsible for tooth shape reside in the ectomesenchyme in specific regions or fields and tell the ectomesenchyme to form a tooth of a specific shape.
A second theory, the
clone theory
, proposes that clones of ectomesenchymal cells are already programmed by the epithelium to become a specific tooth with a specific shape.
Evidence exists to support both theories and it is likely that both may influence tooth development. The Odontogenic Homebox Code (field theory) is based on observing restricted expression of certain homeobox genes (known to be important in tooth development) in early developing ectomesenchyme. It has been observed that expression of Msx1 and Msx2 is restricted to areas of ectomesenchyme corresponding to regions where incisor teeth will eventually develop but not regions where multi-cuspid teeth will develop. Conversely, expression of the genes Dlx-1 and Dlx-2 have been observed in ectomesenchyme corresponding to regions where multi-cuspid teeth, but not single-cusped teeth, form. These areas of expression are broad and overlap, but they may provide the positional information for development of teeth of specific shape in the correct position in the dental arch.
2.6 Amelogenesis
Amelogenesis begins with secretion of a partially mineralised enamel matrix by terminally differentiated ameloblasts until a full thickness of tissue is achieved. This provides an organic scaffold for subsequent mineralisation. This is the secretory phase of amelogenesis. Following this, maturation of secreted enamel matrix is achieved beginning from the amelodentinal junction (ADJ) and proceeding outwards. During this phase there is considerable resorption of the majority of the organic matrix, which is replaced by crystal growth.
The secretory stage begins immediately after dentinogenesis at future cusp tips and following ameloblast differentiation. Ameloblasts secrete an organic enamel matrix which is almost instantly partially mineralised. This first formed enamel matrix is composed of organic, protein matrix (20% by volume), inorganic hydroxyapatite (16% by volume) and water (64% by volume). The organic matrix is comprised of two families of enamel protiens, the amelogenins and the non-amelogenins. The amelogenins are small, soluble hydrophobic proteins and have a significant role in the regulation of enamel prism orientation, enamel mineralisation and crystal growth. The non-amelogenins are a mixture of proteins including enamelin, tuftelin and ameloblastin. Enamelin is a larger, acidic protein encoded by the ENAM gene. Mutations in this gene can give rise to the autosomal dominant amelogenesis imperfecta, suggesting a role for the protein in amelogenesis. Tuftelin is an acidic glycoprotein which has been suggested to have a role in enamel mineralisation, as has ameloblastin.
