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COVER
PREFACE TO THE THIRD EDITION
PREFACE TO THE FIRST EDITION
PART I: THEORY AND APPLICATION IN STUDIESOF PAST PEOPLES
1. CHAPTER 1: BIOARCHAEOLOGICAL ETHICS
  1. INTRODUCTION
  2. THE HISTORY OF BELIEFS ABOUT THE DEAD
  3. THE HISTORY OF RESEARCH ON HUMAN REMAINS
  4. THE SOURCES OF SKELETAL COLLECTIONS
  5. THE VALUE OF HUMAN SKELETAL REMAINS
  6. ETHICAL RESPONSIBILITIES OF SKELETAL BIOLOGISTS
  7. SOURCES OF CONFLICT OVER QUESTIONS OF DESCENDANT RIGHTS
  8. RESOLVING CONFLICTS AND FINDING MUTUALLY BENEFICIAL OUTCOMES
  9. REFERENCES
2. CHAPTER 2: FORENSIC ANTHROPOLOGY
  1. HISTORICAL DEVELOPMENT
  2. RELATIONSHIP OF FORENSIC ANTHROPOLOGY TO SKELETAL BIOLOGY
  3. THEORETICAL ISSUES
  4. THE FORENSIC DATA BANK
  5. EVIDENCE RECOVERY
  6. NONHUMAN VERSUS HUMAN REMAINS
  7. AGE AT DEATH
  8. SEX (NOT GENDER [WALKER AND COOK, 1998])
  9. ANCESTRY
  10. LIVING STATURE
  11. FACIAL APPROXIMATION
  12. PHOTOGRAPHIC SUPERIMPOSITION
  13. TIME SINCE DEATH
  14. POSITIVE IDENTIFICATION
  15. MOLECULAR APPROACHES
  16. EVIDENCE OF FOUL PLAY
  17. FUTURE PROSPECTS
  18. CASE STUDY
  19. REFERENCES
3. CHAPTER 3: TAPHONOMY AND THE NATURE OF ARCHAEOLOGICAL ASSEMBLAGES
  1. TAPHONOMY AS ASSEMBLAGE HISTORY
  2. MORTUARY PROGRAMS AND THE ARCHAEOLOGICAL RECORD
  3. ARCHAEOLOGICAL RECOVERY OF HUMAN REMAINS
  4. EXTRINSIC FACTORS IN BONE PRESERVATION
  5. INTRINSIC FACTORS IN BONE PRESERVATION: SIZE, SHAPE, DENSITY
  6. PRESERVATION, BONE DENSITY, AND CHILDREN IN THE BIOARCHAEOLOGICAL RECORD
  7. PRESERVATION AND PALEOPATHOLOGY
  8. ANIMAL MODIFICATION OF HUMAN BONE
  9. DOCUMENTING ASSEMBLAGES: CONTEXT, PRESERVATION, DEMOGRAPHY, DEPOSITION
  10. HUMAN AGENTS AND HUMAN INTENTIONS IN BONE MODIFICATION
  11. INTERPRETING TAPHONOMY
  12. CONCLUSION
  13. REFERENCES
PART II: MORPHOLOGICAL AND DEVELOPMENTAL ANALYSES
1. CHAPTER 4: CHILDREN IN BIOARCHAEOLOGY
  1. INTRODUCTION
  2. PRESERVATION
  3. SEX DETERMINATION
  4. AGE ESTIMATION
  5. GROWTH AND DEVELOPMENT
  6. PEDIATRIC PALAEOPATHOLOGY
  7. FUTURE DIRECTIONS
  8. CONCLUSIONS
  9. ACKNOWLEDGEMENTS
  10. REFERENCES
2. CHAPTER 5: HISTOMORPHOMETRY OF HUMAN CORTICAL BONE
  1. INTRODUCTION
  2. THE PHYSIOLOGIC BASIS FOR HISTOMORPHOMETRIC AGE‐ESTIMATION TECHNIQUES: BONE MODELING AND REMODELING
  3. CORTICAL BONE HISTOMORPHOLOGY AND AGE ESTIMATION
  4. EFFECTS OF INTRINSIC AND EXTRINSIC VARIABILITY ON HISTOMORPHOMETRIC AGE ESTIMATES
  5. EVALUATION OF HISTOLOGICAL AGE ESTIMATION METHODS
  6. CONCLUSIONS: FUTURE DIRECTIONS AND CONSIDERATIONS IN HISTOLOGICAL AGE ESTIMATION
  7. REFERENCES
  8. APPENDIX A: WORKED EXAMPLES OF TWO AGE ESTIMATION METHODS
  9. APPENDIX B: PROFILE OF SELECTED AGE‐ESTIMATION METHODS
3. CHAPTER 6: BIOMECHANICAL ANALYSES OF ARCHAEOLOGICAL HUMAN SKELETONS
  1. “WOLFF’S LAW” AND BONE FUNCTIONAL ADAPTATION
  2. METHODS FOR ANALYZING LONG‐BONE DIAPHYSEAL STRUCTURE
  3. EVOLUTIONARY TRENDS IN LONG BONE ROBUSTICITY
  4. VARIATION WITHIN RECENT HUMAN POPULATIONS
  5. VARIATION WITHIN INDIVIDUALS
  6. CONCLUSIONS AND FUTURE DIRECTIONS
  7. REFERENCES
4. CHAPTER 7: INCREMENTAL STRUCTURES IN TEETH: KEYS TO UNLOCKING AND UNDERSTANDING DENTAL GROWTH AND DEVELOPMENT
  1. INTRODUCTION
  2. BACKGROUND
  3. DENTAL ANATOMY AND THE HISTOLOGY OF TOOTH GROWTH
  4. DENTAL MICROSTRUCTURAL GROWTH MARKERS
  5. PREPARING TEETH FOR HISTOLOGICAL EXAMINATION
  6. AGE ESTIMATION AND TIMING OF DEVELOPMENTAL EVENTS
  7. NONINVASIVE ESTIMATES UTILIZING PERIKYMATA
  8. USING SHORT‐PERIOD AND LONG‐PERIOD MARKERS
  9. APPLICATIONS AND CHALLENGES
  10. OTHER HISTOLOGICAL APPROACHES
  11. CONCLUSIONS AND FUTURE RESEARCH DIRECTIONS
  12. ACKNOWLEDGEMENTS
  13. REFERENCES
5. CHAPTER 8: DENTAL MORPHOLOGY
  1. INTRODUCTION
  2. A BIT OF HISTORY
  3. FUNDAMENTAL ISSUES
  4. METHODS
  5. POPULATION STUDIES
  6. CONCLUDING THOUGHTS
  7. REFERENCES
PART III: PREHISTORIC HEALTH AND DISEASE
1. CHAPTER 9: DENTAL PATHOLOGY
  1. INTRODUCTION
  2. DEFECTS OF DENTAL DEVELOPMENT IN THE ENAMEL OF THE TOOTH CROWN
  3. TOOTH WEAR: CHIPPING AND FRACTURES
  4. PLAQUE‐RELATED DISEASES
  5. THE PLACE OF DENTAL PALAEOPATHOLOGY IN ARCHAEOLOGY
  6. SUGGESTED SCORING SCHEMES FOR CARIES AND PERIODONTAL DISEASE
  7. REFERENCES
2. CHAPTER 10: ANALYSIS AND INTERPRETATION OF TRAUMA IN SKELETAL REMAINS
  1. INTRODUCTION
  2. OSSIFICATION OF SOFT TISSUES
  3. EXTRINSICALLY INDUCED ABNORMAL SHAPE OR CONTOUR
  4. SKULL FRACTURES
  5. FACIAL FRACTURES
  6. FRACTURES OF FLAT AND IRREGULAR BONES
  7. LONG BONE FRACTURES
  8. BLUNT AND SHARP FORCE TRAUMA
  9. FRACTURE HEALING
  10. INTERPRETING THE CAUSE OF INJURY
  11. ACKNOWLEDGMENTS
  12. REFERENCES
3. CHAPTER 11: UNDERSTANDING BONE AGING, LOSS, AND OSTEOPOROSIS IN THE PAST
  1. INTRODUCTION
  2. GROWTH, AGING AND BONE LOSS
  3. SORTING OUT THE INFLUENCES ON BONE MAINTENANCE IN THE PAST
  4. UNIQUE CHALLENGES TO DIAGNOSIS IN ARCHAEOLOGICAL POPULATIONS
  5. FUTURE DIRECTIONS: WHAT BONE LOSS IN THE PAST REALLY MEANS
  6. REFERENCES
4. CHAPTER 12: INFECTIOUS AND METABOLIC DISEASES: A SYNERGISTIC RELATIONSHIP
  1. INTRODUCTION
  2. METHODS OF ANALYSIS FOR METABOLIC AND INFECTIOUS DISEASES
  3. SYNERGISTIC RELATIONSHIPS BETWEEN METABOLIC AND INFECTIOUS DISEASES
  4. CONCLUSIONS
  5. ACKNOWLEDGEMENTS
  6. REFERENCES
5. CHAPTER 13: PALEOPATHOLOGY: FROM BONES TO SOCIAL BEHAVIOR
  1. INTRODUCTION
  2. FOUNDATIONS OF PALEOPATHOLOGY
  3. INFERING BEHAVIOR FROM BONES
  4. LOOKING TOWARD THE FUTURE
  5. REFERENCES
PART IV: CHEMICAL AND GENETIC ANALYSES OF HARD TISSUES
1. CHAPTER 14: STABLE ISOTOPE ANALYSIS: A TOOL FOR STUDYING PAST DIET, DEMOGRAPHY, AND LIFE HISTORY
  1. INTRODUCTION
  2. BASIC CONCEPTS OF STABLE ISOTOPE VARIATION
  3. MASS SPECTROMETRY
  4. APPLICATION OF STABLE ISOTOPE ANALYSIS TO SELECTED PROBLEMS IN SKELETAL BIOLOGY
  5. RESIDENCE AND MIGRATION STUDIES
  6. A DAY WITHOUT STABLE ISOTOPES: WHAT HAS THEIR USE ADDED TO OUR KNOWLEDGE?
  7. ACKNOWLEDGEMENTS
  8. REFERENCES
2. CHAPTER 15: STRONTIUM ISOTOPES AND THE CHEMISTRY OF BONES AND TEETH
  1. THE MINERAL FRACTION OF HARD TISSUES
  2. STRONTIUM ISOTOPES
  3. APPLICATIONS IN BIOLOGICAL ANTHROPOLOGY
  4. REFERENCES
3. CHAPTER 16: ANCIENT DNA ANALYSIS OF ARCHAEOLOGICAL REMAINS
  1. INTRODUCTION
  2. METHODS
  3. CASE EXAMPLES
  4. CONCLUSIONS AND FUTURE PROSPECTS
  5. REFERENCES
PART V: QUANTITATIVE METHODS AND POPULATION STUDIES
1. CHAPTER 17: TRADITIONAL MORPHOMETRICS AND BIOLOGICAL DISTANCE: METHODS AND AN EXAMPLE
  1. BACKGROUND
  2. METRIC ANALYSES
  3. MODEL‐BOUND AND MODEL‐FREE APPROACHES
  4. ASSUMPTIONS OF MULTIVARIATE DATA
  5. CLASSIC MULTIVARIATE STATISTICAL PROCEDURES
  6. AN EXAMPLE
  7. CONCLUSIONS AND FUTURE DIRECTIONS
  8. ACKNOWLEDGMENTS
  9. REFERENCES
2. CHAPTER 18: PALEODEMOGRAPHY: PROBLEMS, PROGRESS, AND POTENTIAL
  1. INTRODUCTION
  2. POINT–COUNTERPOINT
  3. STORIES SKELETONS CAN TELL
  4. SKELETONS AS A SAMPLE OF DEATHS
  5. MEASUREMENT CONCERNS
  6. ANALYTICAL CONCERNS
  7. PALEODEMOGRAPHY AND RELATED FIELDS
  8. CONCLUSION
  9. ACKNOWLEDGMENTS
  10. REFERENCES
INDEX
END USER LICENSE AGREEMENT

List of Tables

Chapter 03
1. TABLE 3.1 Stages in the history of an Archaeological Skeletal Assemblage
2. TABLE 3.2 Variables in Recording Mortuary Features
3. TABLE 3.3 Subadults in Burial Clusters, Guam Hyatt site
4. Table 3.4 Examples of variables in taphonomy Data Collection Protocol from White 1992 (With Additions from Knüsel and Outram 2004, and Stodder and Osterholtz 2010)
5. TABLE 3.5 Taphonomic Alterations Characteristic of Secondary Burial and victims of conflict, Southern Plains
6. TABLE 3.6 Taphonomic profiles of Primary Burials, Cannibalized Human Remains, Mammal Remains, and Secondary Burials from Fiji and New Guinea
Chapter 04
1. TABLE 4.1 Documented Child Skeletons
2. TABLE 4.2 Skeletal and Dental Features Associated with the stages of maturation in boys and girls
Chapter 05
1. TABLE 5.1 Variation in Secondary Osteon Definitions Used by Different Authors
2. TABLE 5.2 Variation in reports of association between Histomorphological Features and age*
3. TABLE 5.3 Subadult Age Categories Based Upon Cortical Bone Histomorphology
Chapter 06
1. TABLE 6.1 Biomechanical studies of Human Long Bone Diaphyses in an Anthropological Context through 2016
2. TABLE 6.2 Definitions of Cross‐sectional Geometric Properties
Chapter 09
1. TABLE 9.1 Caries Susceptibility in Children’s Permanent Tooth Crowns
Chapter 10
1. TABLE 10.1 Fracture Types and Mechanisms of Injury (Adapted From Lovell 1997; Galloway et al. 2014). Types 1 Through 4 are Caused by Direct Trauma; Types 5 Through 14 are Due to Indirect Trauma
2. TABLE 10.2 Summary of Fracture Healing in Adult Tubular Bone (after Buchwalter et al., 2006; Schenk, 2003; Shantz et al., 2015)
Chapter 11
1. TABLE 11.1 Some Methods that Can be Used in the Study of Bone Loss and Osteoporosis in Archaeological Skeletal Samples. (For Extensive Reviews of Paleopathological Studies of Bone Loss and Fragility and Methodology see Agarwal and Grynpas 1996, Brickley and Agarwal 2003, Curate 2014, Ives et al. 2017, Nelson et al. 2015)
2. TABLE 11.2 Some Secondary Causes of Osteoporosis (NIH/ORBD 2006; Miazgowski et al., 2012; Riggs et al. 1991)
3. TABLE 11.3 Some Currently Suggested Risk Factors for Osteoporosis. Modified from Riggs et al. (1991) and the National Osteoporosis Foundation (2006)
Chapter 14
1. TABLE 14.1 Average Terrestrial Abundances of Stable Isotopes of Elements Used in Analyses of Ancient Human Tissues (Extracted from Table 1.1 of Ehleringer and Rundel 1989)
2. TABLE 14.2 Primary (International) and Reference Standards for Selected Elements (From Hoefs 1997 and Coplen 1994)
Chapter 17
1. TABLE 17.1 Fifty‐six Male Cranial Series Used in the Example
2. TABLE 17.2 Summary Ranking of Cranial Measurements According to F‐Values Received in the Final Step of Discriminant Function Analysis (56 Male Groups, 27 Measurements)
3. TABLE 17.3 Eigenvalues, Percentage of Total Dispersion, Cumulative Percentage of Dispersion, and Level of Significance for 27 Canonical Variates Resulting from Stepwise Discriminant Function Analysis (56 Male Groups, 27 Measurements)
4. TABLE 17.4 Canonical Coefficients of 27 Cranial Measurements for the First Three Canonical Variates that Result from Stepwise Discriminant Function Analysis Using 56 Male Groups
5. TABLE 17.5 Classification Results (Regular and Jackknifed) Arranged by Groups With the Best to the Poorest Results Showing Percentage of Correctly Assigned Cases
6. TABLE 17.6 Some of the Jackknifed Classification Results Obtained From Stepwise Discriminant Function Analysis Showing the Cases Reclassified at the End of the Stepping Process (Numbers in Parentheses Represent the Number of Crania Originally Assigned to Each Group). See Table 17.1 For Explanation of Abbreviations
7. TABLE 17.7 The Smallest Mahalanobis Distances for 56 Male Cranial Groups Using 27 Measurements. All Distances are Significant P < 0.01 Unless Indicated Otherwise

List of Illustrations

Chapter 03
1. Figure 3.1 Bone mineral density (circumference) for the humerus and tibia.
2. Figure 3.2 Periosteal new bone chipping off an infant tibia.
3. Figure 3.3 Rodent gnawing, mandible.
4. Figure 3.4 Element representation based on MNI of 33; MNIs per element or element group in subadults and in the total PHR assemblage from Feature 104, Sacred Ridge site.
5. Figure 3.5 GIS‐generated distribution of cranial bone fragments in pit house Feature 104, Sacred Ridge site. Stodder et al. 2010:306 fig. 13.19. Used with permission of SWCA Environmental Consultants, Inc.
6. Figure 3.6 Femur zones used to record tool mark locations. Stodder and Osterholtz 2010:265 fig. 12.12, and 2010:264 table 12.18. Used with permission of SWCA Environmental Consultants, Inc.
7. Figure 3.7a Defleshed secondary burial, Boundary Mound Burial 6 (after Olsen and Shipman 1994:380 fig. 5).
8. Figure 3.7b Cut marks, cranial trauma, perimortem fractures (no defleshing), a Bronze Age trauma victim (after Outram et al. 2005:1706 fig. 6).
9. Figure 3.7c Cut marks on defleshed skeleton (no disarticulation), Alfred Packer historic cannibalism assemblage (after Rautman and Fenton 2006:331 fig.6).
10. Figure 3.7d Composite distribution of tool marks on processed individuals, Sacred Ridge Site.
11. Figure 3.8a Scalping, Larson Site Burial 62B (after Olsen and Shipman 1994:383 fig. 8).
12. Figure 3.8b Defleshing for secondary burial, Split Rock Creek Burial 8 (after Olsen and Shipman 1994:381 fig 6).
13. Figure 3.8c Cut marks typically found on Aztec sacrifice victims and temporal perforations on a skull prepared for mounting on a skull rack (tzompantli) (after Pijoan Aguade and Lory 1997:231 fig. 8.8).
14. Figure 3.8d Curated skull from Ibunda, Lower Sepik, Papua New Guinea. Incised design on parietals, pitch and clay on frontal, holes drilled for attaching mandible and for hanging skull, defleshing marks, cuts from fiber ties, orbit and nasal damage from pith eyes and nose.
15. Figure 3.9 Fracture types in long bone shafts
16. Figure 3.10 Proximal femur conjoin with differential burning, cut marks, V and spiral fractures. Photograph from Stodder et al. 2010:402 fig. 13.95 with additional unpublished data, used with permission of SWCA Environmental Consultants, Inc.
Chapter 04
1. Figure 4.1 (a) Skeletal remains of a Romano‐British perinate bagged by the archaeologist on‐site. (b) Skeletal remains of the same perinate after the bagged surrounding soil was examined. Note the significantly greater recovery of the centra (vertebral bodies), hands and feet.
Chapter 05
1. Figure 5.1 (a): During development, modeling drifts in the middle third of the sixth rib remove bone from the internally facing surfaces and deposit bone on the externally facing surfaces. As the rib drifts laterally, the formation surfaces outpace the resorptive surfaces, and the rib gains cross‐sectional area. Note that none of the tissue present in the young rib (a) is present in the adult rib (c); it has been completely “modeled out.” (b): Enlarged view of the drifting rib cortex (trabeculae have been removed for clarity). The younger bone (lamellae) is darker, and the older bone is lighter. The cross section thus comprises a mosaic of different aged lamellae. (c): The same drifting rib cortex illustrated in B. The stippled region represents the size and position of the rib cortex at time 1 (arbitrarily designated as age 6 in the figure). A year later (shaded silhouette), some of the cortex that was present at age 6 is still present (region exhibiting both stippling and shading). However, nearly half of the cortical bone present at age 7 did not exist in the same rib just one year earlier. Bone modeling is a dynamic process in the growing skeleton that regularly and rapidly alters the size, shape, relative position, and age of bone tissue.
2. Figure 5.2 (a) Undecalcified cross section of a tibial diaphysis illustrating cortical histomorphology. Cross (†) = circumferential (primary) lamellar bone. Solid arrow (→) = type I (common) osteons. Feathered arrow (➳) = type II osteon. Darts (➸) = osteon fragments. Asterisk (*) = resorptive bay. Open arrow () = drifting osteon. Open point (➢) = primary osteon. Closed point () = primary vascular canal (non‐Haversian canal). (b) Microradiograph from an ulnar diaphysis illustrating a double‐zonal osteon (center). Note that the arrest line (lighter ring) follows the contours of the centripetal lamellae and osteocyte lacunae.
3. Figure 5.3 (top) Longitudinal view of a basic multicellular unit (BMU) moving through tissue space from right to left. (bottom) Schematic illustrations of an evolving osteon corresponding to selected transverse sections of the longitudinal system depicted above. Redrawn after Stout (1989).
Chapter 06
1. Figure 6.1 A simple feedback model of bone functional adaptation (after Lanyon 1982).
2. Figure CE1 Cross‐sectional properties (see Table 6.2 for definitions and units).
3. Figure CE2 Declining mobility and long bone strength in Europe.
4. Figure 6.2 Changes in cross‐sectional shape of the femoral diaphysis with the transition to agriculture on the Georgia coast.
5. Figure 6.3 Effects of terrain on femoral midshaft robusticity (polar second moment of area, standardized for bone length and controlled for subsistence strategy and sex) in Native North American archaeological samples. Mean ± 1 SE.
6. Figure 6.4 Combined measure of humeral diaphyseal strength standardized for body size (see text) in Native North American non‐rowing, river‐rowing, and ocean‐rowing population samples.
7. Figure 6.5 Relative femoral and humeral midshaft rigidity (polar section modulus standardized for body size) in Andamanese Islanders and South Africans. Mean ± 1 SD.
8. Figure 6.6 Sexual dimorphism [(male–female)/female⋅ 100)] in femoral midshaft A‐P to M‐L bending rigidity (second moments of area) in relation to subsistence strategy. Filled and open squares: Native North Americans; circles: modern Japanese and US whites; filled star: Neandertals; open star: Upper Paleolithic humans.
9. Figure 6.7 Age changes and sex differences in mid‐distal femoral diaphyseal A‐P to M‐L bending rigidity (second moments of area) in the Pecos Pueblo sample. Small filled circles: unsexed juveniles; open squares: adolescent males; filled circles: adolescent females; large open square and filled circle: mean ± 1 SD for 20–24 year old males and females, respectively. (See Ruff et al. 1994 for sample details.)
10. Figure CE3 Skeletal variability in bone strength changes during growth.
11. Figure 6.8 Age changes in geometric section properties of the femoral midshaft in the entire Pecos Pueblo sample. Sexes combined. (See Ruff and Hayes 1983a and Ruff et al. 1994 for sample details).
12. Figure 6.9 Schematic representation of age changes in cortical geometry among adults from Pecos Pueblo and a modern U.S. white sample.
13. Figure 6.10 Bilateral asymmetry [median of (maximum–minimum)/minimum) × 100] of humeral shaft strength (polar section modulus) and distal articular size (articular breadth²) in modern (Euroamerican and tennis players), archaeological, and paleontological (Neandertal and Upper Paleolithic) samples, arranged in order of shaft strength asymmetry. Question mark indicates no data available.
14. Figure CE4 Temporal changes in humeral strength asymmetry in Europe.
Chapter 07
1. Figure 7.1 A tooth and its supporting tissues, illustrating some of the internal microstructures of enamel and dentine. A small section of enamel has been magnified to show the relationship between enamel prisms that follow a course from the EDJ to the enamel surface, and striae of Retzius that cross cut prisms at an angle. The inset micrograph relating to the schematic (b) shows an actual longitudinal enamel section examined under polarized light, with prisms running from right to left and three brown striae of Retzius cross‐cutting them diagonally from bottom right to top left. Cross‐striations, marking daily appositional increments, can be clearly seen as cross‐banding on the prisms in this photograph. The same number of cross‐striations can be counted between all adjacent regular striae in one tooth, and this circaseptan interval is also identical in all of the teeth in one dentition. The schematic (a) shows one prism highly magnified (the dotted line from the sketch leads to a schematic prism in box (b)), with cross‐striations illustrated as dark bands on prism varicosities. Note that one cross striation in this context is defined as running from the end of one dark band to the beginning of another. The inset photomicrograph relating to the prism in box (a) is a taken with a scanning electron microscope (SEM) and it shows a small portion of enamel fractured in an oblique transverse plane. A number of prisms and their three‐dimensional relationship to each other can be seen, as well as the varicosities on each prism, which are cross‐striations as they appear in the SEM. The schematic (c) at the bottom of the figure depicts a section of dentine, with long‐period Andresen lines running diagonally from lower left to upper right and dentine tubules cross cutting them obliquely. The photomicrograph relating to (c) is a longitudinal section taken in polarized light.
2. Figure 7.2 Schematic illustrating striae of Retzius and perikymata in three views. Top left (a) is a transverse section through a tooth in which striae appear as concentric rings. Top right (b) is a view looking at the outside surface of the crown in which perikymata appear as ridges encircling it. The inset is an actual photograph of perikymata. On the bottom (c) is a longitudinal section showing striae as continuous domes around the dentine horn. The first discontinuous layer to emerge at the surface terminates as a perikyma, and striae and perikymata continue down either side of the crown to the cervix. The inset photomicrograph is a longitudinal section of enamel.
3. Figure 7.3 The general pattern of incremental growth illustrating formation of some of the many long‐period lines in enamel and dentine (up to the end of crown formation). Growth begins with initial dentine deposition at (a) and proceeds through to the early stages of crown formation at (e). In reality, the growth lines are more closely packed in the cervical enamel.
4. Figure 7.4 Schematic drawing representing a way of conceptualizing long‐period incremental growth lines. The upper two diagrams show two aspects of the lower diagram, which represents the cuspal area of a tooth sectioned longitudinally. Diagram (a) illustrates a few of the many enamel prisms that run from the EDJ to the surface, drawn schematically as straight lines. Diagram (b) decouples striae of Retzius from prisms, envisioning them as an epiphenomenon superimposed on prism growth. Diagram (c) is (b) overlaid on (a).
5. Figure 7.5 This scheme classifies the major microstructures of enamel (the list of microstructures is not exhaustive and excludes, for instance, intradian lines and laminations). See the text for a detailed explanation.
6. Figure 7.6 Schematic illustrating Boyde's histological age‐estimation technique. The two outline drawings are longitudinal sections of teeth, the upper a mandibular first molar and the lower a mandibular central incisor. The numbers are cross striation counts. The dotted lines represent accentuated striae of Retzius that could be identified in both teeth. The vertical lines labelled, e.g. AA', represent prisms. Boyde in fact used more prisms than shown, but those illustrated demonstrate the technique using the identifiable accentuated Retzius lines. Cross‐striations are first counted from the neonatal line in M1 out to the surface along prism AA'. Note that when the ameloblast forming prism AA' reached the surface at A', the incremental layer was situated along the Retzius line approximated by AB', and the next ameloblast to start secreting enamel was at point B. Therefore the next cross striation count is made along prism BB', the next along CC' and so on. Looking at the lower drawing the pattern of significant striae shows the same cross striation counts up to the incremental line at 1122. Counting is then continued until the final total of 1692 days is reached. This is the point where enamel formation ceased at death (After Boyde 1963).
7. Figure 7.7 Schematic diagram of a longitudinally sectioned tooth showing derivation of formula for calculating total crown formation time and the timing of developmental events, like Wilson bands.
8. Figure 7.8 A longitudinal photomicrograph (at 200× magnification) of enamel, showing how cross‐striations (which have been marked by thin white lines) can be tracked across a series of striae and transferred from one striae to another so that clearer fields of view are utilized (Dean and Beynon 1991). This technique enables researchers to avoid areas where the structures are not clearly visible.
Chapter 08
1. Figure 8.1 A common sight in archaeological contexts – well preserved teeth mixed in with highly fragmented bone. The hydroxyapatite of enamel is primarily inorganic, so teeth usually preserve better than bone in the archaeological and paleontological record.
2. Figure 8.2 The upper molar field with the hypocone of UM1 and UM2; UM3 is dysmorphic, but the small distolingual cone is probably a form of hypocone expression. Black arrows point to cusp 5 on UM1 and UM2; both the hypocone and cusp 5 are significantly larger on UM1.
3. Figure 8.3 Tuberculum dentale, expressed as ridges and/or tubercles on UI1 and UI2 (intratrait, intrafield interaction) and UC (intratrait, interfield interaction).
4. Figure 8.4 Ranked scale for canine tuberculum dentale; note absence of trait for grade 0 and pronounced expression of tubercle on grade 7. Intermediate ranks approximate even spacing between any two grades. Only left upper canines were used in this classification.
5. Figure 8.5 When shoveling in American Indians is scored on the Hrdlička/Dahlberg four‐grade scale, its distribution is strongly skewed to the right. When this trait is scored on the basis of an eight‐grade scale (0 and 7 degrees of presence), the distribution in Southwest Indians is almost normal.
6. Figure 8.6 Pronounced bilateral winging in an American Indian dentition; incisors also exhibit grade 3 shoveling expression.
7. Figure 8.7 The maxillary dentitions of a European (a) and American Indian (b) showing the two extremes of upper incisor shoveling variation. In both dentitions, UI1 and UI2 exhibit comparable levels of lingual marginal ridge development.
8. Figure 8.8 Interruption grooves on UI1 and UI2 (black arrows); the groove crosses both the crown and root on the right UI2, hence the alternative name of coronoradicular groove.
9. Figure 8.9 The Uto‐Aztecan premolar is a rare variant of UP1 found primarily in Native Americans; note the strong buccalward rotation of the buccal cusp and large pit separating the buccal and lingual cusps. The large tubercle between the lingual cusp and pit (black arrow) is unusually large for this trait.
10. Figure 8.10 The left LP2 exhibits an odontome; this conical cusp centered in the sagittal sulcus is worn, showing dentine involvement in its formation.
11. Figure 8.11 Variation in the expression of Carabelli’s trait. (a) and (b) show absence and pit expressions, respectively, while (c) and (d) exhibit moderate and pronounced cusp formations. Although low grades of expression can be obscured by wear on the protocone, large grade 7 cusps are still evident even after extensive wear as shown in (e).
12. Figure 8.12 Two rooted lower canines can often be scored even when the tooth is missing. The vacated lower canine shows the presence of two distinct root sockets. In this case, the two‐rooted tooth was also available.
13. Figure 8.13 Lower premolars always have a prominent buccal cusp but lingual cusps vary in both size and number. In (a), both LP1 and LP2 effectively lack a lingual cusp; by contrast, (b) shows cases where LP1 exhibits two cusps and LP2 has three distinct lingual cusps.
14. Figure 8.14 Lower molars have five major cusps that are both numbered and named. The buccal cusps are odd numbered while the lingual cusps are even numbered. The names given to these cusps by mammalian paleontologists are still used even though new terminologies have been recommended (1 = protoconid; 2 = metaconid; 3 = hypoconid; 4 = metaconid; 5 = hypoconulid). Note the high degree of symmetry and mirror imagery between the left and right lower first molars.
15. Figure 8.15 An extremely large cusp 7 is located between the metaconid and entoconid of the lower first molars (white arrows). At one time, it was thought the post‐metaconulid was a manifestation of cusp 7, but the post‐metaconulid and cusp 7 can both be expressed on the same tooth. For this reason, grade 1A of the ASUDAS plaque series should not be considered part of cusp 7 variation.
16. Figure 8.16 A mixed dentition with dm1, dm2 and UM1 shows that the morphology of the second deciduous molar often anticipates the expression of traits on the permanent first molar. In this example, both dm2 and UM1 exhibit distinct manifestations of Carabelli’s trait.
Chapter 09
1. Figure 9.1 Interrelationships of different dental conditions.
2. Figure 9.2 A lower canine showing different forms of enamel hypoplasia which greatly disrupt the shape of the crown. There are plane‐form defects, some pitted defects and furrow‐form defects, and combinations of the two. This is an epoxy resin replica, cast from a Coltene President dental impression, sputter coated in gold and examined in the scanning electron microscope. Two images have been merged together to show the full crown height. Some of the pitted defects have bubbles in them, trapped during the taking of the impression.
3. Figure 9.3 Formation sequence for crown surfaces of all permanent teeth, except premolars. Redrawn from figures 3 and 4 in Reid and Dean (2006). The crown surfaces are each divided into 10 equal zones of crown height and the mean ages at which they were formed determined by counting cross striations and brown striae of Retzius in sections under an optical microscope. The ages are quoted in years after birth. For most, two ages are quoted, separated by a slash. The first age was determined from a sample of teeth from southern Africa. The second age was determined from a tooth sample from northern Europe. Where only one figure is given, the two samples provided identical results. It is possible to use the sequence to estimate the ages at which furrow‐form defects were initiated by drawing on the positions of the defects for different teeth. Ages can be confirmed by matching the position of defects on one tooth with another.
4. Figure 9.4 Two views of a left upper jaw from an Anglo‐Saxon site in Winchester, England. (a) The central part of the occlusal surface in the molars has been worn away to expose the softer dentine, leaving a higher rim of the harder enamel. (b) Approximal attrition has broken through the mesial and distal sides of this rim in the first molar, and has thinned it on these sides in the second molar. The second premolar was fractured during life, and subsequently become worn. There is little evidence of bone loss from periodontal disease, but remodeling of the alveolar process has led to thinning of the buccal plate. This is particularly evident over the sockets of the incisors, canines and premolars, which bulge outwards. The first molar is loose and has dropped down slightly in the lower picture (b), to reveal an opening into the smooth‐walled cavity of a periapical granuloma around the apex of its distobuccal root. The wafer‐thin opening suggests that the granuloma has been exposed by a fenestration due to the buccal plate thinning, and not by the sinus of an abscess. There is no sign of an open pulp chamber or root canal on the worn occlusal surface of this tooth, so it may be that a fine crack allowed the pulp to be infected. In the fractured second premolar there is also no evidence of root canal exposure or periapical inflammation, and the fenestration which exposes the root surface must again be due to general remodeling of the buccal plate. The exposed root surfaces are roughened and bulbous, suggesting hypercementosis. Eroded remnants of supragingival calculus are visible on the roots of the molars. This specimen is in the collection of the Natural History Museum, London, and has been photographed with their permission.
5. Figure 9.5 Diagrammatic internal structure of the mandible of a young adult (the third molar is still erupting), seen as a section along the mandibular body and showing the mandibular canal. Each socket is separated from the others by an interdental “wall” consisting of the alveolar bone layers lining the sockets and the intervening trabecular bone. The Kerr (1991) score for periodontal disease is assigned on the basis of the alveolar crest at the top of this interdental wall. The four smaller diagrams are all transverse sections of the mandibular body at the position of the third premolar. (a) is the form expected in a young adult, with little worn teeth and no evidence of periodontal disease. (b) is an older adult, in which there has been occlusal attrition and continuous eruption of the teeth so that the roots are exposed, and the apex is further away from the inferior alveolar canal, but the height of the body has not been diminished. (c) is the same wear and eruption state, with pulp penetration from a large carious lesion on the root surface, resulting in bone remodeling around the root apex due to periapical inflammation. The periapical cavity has grown so large that it has breached the cortical bone plate on the buccal side to create a fenestration. (d) is a young adult in which periodontal disease has caused loss of the alveolar bone which lines the tooth socket. The mandibular canal makes a convenient measuring point for the position of the tooth sockets, so that the effects of continuous eruption can be monitored in the worn dentition of the older adult. Outlines of sections based upon diagrams in Brescia, N.J. (1961) Applied dental anatomy, St. Louis: Mosby.
6. Figure 9.6 Lower first molar, premolars and canine of a post‐medieval jaw from London. Either side, the empty sockets denote teeth which have been lost postmortem. Alveolar bone (lining the socket) has been lost around the roots of the molar and, most noticeably in this view, the second premolar to create a deep crater between it and the molar. This is the classic appearance of bone loss due to periodontal disease. The crests of the interdental plates between other teeth are much less affected, but are still somewhat porous. Along the CEJ of all four teeth is a lesion that looks very much like root‐surface caries but, in archaeological material like this, it is important to consider possible diagenetic effects.
7. Figure 9.7 Gross approximal caries which has destroyed the mesial side of an upper incisor in an early medieval skull from London. The lesion may well have been initiated at the contact point but has advanced so far that it is not possible to be sure.
8. Figure 9.8 Two views of part of the right upper jaw from an Anglo‐Saxon skull from Winchester, England. Upper view (a) shows the buccal side of the same specimen. The thinned buccal plate of the alveolar process has broken away (the sharp broken edge is clearly visible) to reveal the smooth cavities of two periapical granulomata around the apices of the buccal roots of the molar. There are eroded remnants of supragingival calculus on the crown and roots of the first molar and first premolar. Lower view (b) shows a gross gross lesion (so large that it cannot reliably be distinguished as coronal in origin) which has exposed the open root canal of the upper first molar. The second premolar next to it has been lost postmortem. This specimen is in the collection of the Natural History Museum, London, and has been photographed with their kind permission.
Chapter 10
1. Figure 10.1 The two common types of traumatic injury in children, the greenstick or longitudinal fracture (left) and the torus or buckling fracture (right).
2. Figure 10.2 Fractures caused by direct trauma, from left to right: transverse, penetrating, and comminuted.
3. Figure 10.3 Fractures caused by indirect trauma, from left to right: oblique, spiral, and impacted.
4. Figure 10.4 Avulsion fracture of the patella.
5. Figure 10.5 Typical cranial vault fractures, from left to right: linear, depressed, and penetrating.
6. Figure 10.6 Depressed cranial fracture.
7. Figure 10.7 Le Fort fractures of the face.
8. Figure 10.8 Fracture of the vertebral body caused by herniation of the intervertebral disk.
9. Figure 10.9 Crush fracture of the anterior vertebral body, producing a wedge shape.
10. Figure 10.10 An impacted metacarpal fracture resulting from compressive force.
11. Figure 10.11 Healing spiral fracture of a phalanx.
12. Figure 10.12 Evidence of fracture and dislocation at the shoulder: the head of the humerus was dislocated anteriorly and medially and was crushed against the rim of the glenoid fossa. A healed fracture is evident at the neck of the humerus, and a secondary “articular” surface has formed on the anterior surface of the scapula. Given the crushing injury to the humeral head against the rim of the glenoid fossa, movement would have been greatly restricted and the arm held in an abnormal position.
13. Figure 10.13 The Salter–Harris classification system for fractures of juvenile long bones.
14. Figure 10.14 A Colles fracture of the distal radius.
15. Figure 10.15 Fine woven bone indicating healing at a fracture site.
Chapter 11
1. Figure 11.1 Aspects of bone quantity and quality that are known to affect bone fragility and could contribute to risk of osteoporotic fracture. Bone mass or bone mineral density (BMD) is the typical measure of bone quantity. Reduced bone mass is referred to as osteopenia and contributes to risk of fracture. Note, osteopenia may actually be a consequence following or exacerbated by fracture (Heaney 1992). More recently, a number of additional factors grouped as contributors to bone quality, including bone geometry, cortical bone histomorphology, trabecular architecture, and bone material properties (such as collagen amount or organization, bone mineralization or fatigue damage) have been recognized as contributing to bone strength and fragility.
2. Figure 11.2 Scanning electron microscope image (in backscattered electron imaging mode) of human rib sections. Left: modern rib, right: archaeological rib sample. Note the modern rib shows varying gray levels that correlate to normal differing areas of remodeled bone tissue and subsequent mineralization ages. The archaeological rib shows significant diagenetic destruction of both microstructure and chemical alteration of mineralization levels.
Chapter 12
1. Figure 12.1 Periosteal new bone formation on the visceral surfaces of ribs in a skeleton from the Robert J Terry Collection, Smithsonian Institution, Washington DC (see Roberts et al 1994).
2. Figure 12.2 Periosteal new bone formation on the endocranial surface of the skull of a person buried in Norwich, Norfolk, England in the post‐Medieval period
3. Figure 12.3 Examples of pathological changes observed in individuals with suggested co‐occurrence of rickets and scurvy. (a) Porosity and new bone formation present on the scapulae, S514; (b) porosity and flaring (arrows) of the sternal rib ends, S95. See Schattmann et al. (2016) for full discussion of appearance and expression of pathological changes.
4. Figure 12.4 Radiography of the foot of a person with leprosy showing dorsal tarsal “bars.”
5. Figure 12.5 BSE‐SEM image from the rib of a child (1.5yrs +/– 3 months) from the Roman Imperial cemetery of Isola Sacra, Lazio, Italy. The skeleton of the child was too poorly preserved to allow a diagnosis of rickets to be made based on macroscopically visible pathological changes, but the BSE‐SEM image clearly shows incomplete layers of new bone formation and defective mineralization along cement lines, and areas of poorly mineralized new bone formation. Images from a SSHRC funded research project on vitamin D deficiency in the Western Roman Empire. Arrows with black outlines point to areas where new bone formation is poor and is separated from previously formed bone by defective mineralization adjacent to cement lines. The arrows with grey outlines indicate areas of diagenetic change.
6. Figure 12.6 Three children with rickets; anon., Friends' Relief Mission, Vienna XII, n.d. Photograph circa 1920–1930. https://wellcomecollection.org/works?query=L0014375&wellcomeImagesUrl=GET%20/indexplus/image/L0014375.html%20HTTP/1.1. Licensed under CC BY 4.0.
7. Figure 12.7 Mandible of a 12–14‐year‐old child from the post‐medieval Quaker cemetery of Coach Lane, North Shields, England showing destruction and new bone formation; the child may also have had TB, rickets, and scurvy (see Roberts et al 2016).
8. Figure 12.8 Plate from “On a form of chronic inflammation of bones (Osteitis deformans), Medic‐chirurgical transaction,” James Paget 1877. Figures 1–3: patient taken six months before death. Figure 4: cap worn in 1844 and hat worn in 1876. Bowing of tibiae can clearly be seen in Figures 1–3 and cranial expansion is evidenced in Figure 4. http://wellcomeimages.org/indexplus/obf_images/03/e6/295749d90297776546edd592e840.jpg. Licensed under CC BY 4.0.
Chapter 13
1. Figure 13.1 Individual 024 from the Dunning Poorhouse Cemetery, displaying dental restorations.
Chapter 14
1. Figure 14.1 Diagram showing three of the four components of the mass spectrometer: gas is introduced into the source where molecules are ionized then accelerated; the resulting ion beam is directed into the mass analyzer where ions of different masses are separated; ion collectors measure intensities of the separated ion beams.
2. Figure 14.2 δ¹³C and δ¹⁵N values (mean ± one standard deviation) for collagen from human and faunal bone samples from sites in the Sierra Blanca region of New Mexico, dating from CE 800 to CE1400.
3. Figure 14.3 δ¹³C and δ¹⁵N values (means and standard deviations) for collagen from human and faunal bone samples from sites from the western shore of Lake Baikal, dating from the Early Neolithic (5800–4900 BCE) to the Early Bronze Age (3400–1700 BCE). Fish bones are from modern specimens. Mean values for human bones are plotted by site. Sample size is provided in parentheses.
Chapter 15
1. Figure 15.1 Logarithm of Sr/Ca data published by Elias and others (1982) from a food chain in Yosemite, California showing biopurification, in which Sr/Ca drops by a factor of five with each trophic level.
Chapter 16
1. Figure 16.1 The mtDNA genome codes for 13 proteins (or subunits of proteins), two ribosomal RNA subunits, and 23 transfer RNAs (necessary because the mtDNA genetic code is slightly different than the nuclear genetic code). Different genes are found on the heavy (H) and light (L) strands of the DNA. These are transcribed in opposite directions. From Page and Holmes (1998) Molecular Evolution: a Phylogenetic Approach.
2. Figure 16.2 A normal karyotype for a human male. Public Domain.
3. Figure 16.3 (a) PCR, and (b) electrophoresis.
4. Figure 16.4 Schematic of next‐generation sequencing workflow for ancient DNA samples. 1) DNA extraction; 2) library preparation; 3) shotgun sequencing; 4) array‐based target enrichment; 5) in‐solution based target enrichment; 6) sequencing.
5. Figure 16.5 Characteristic ancient DNA degradation patterns due to deamination. Plots show high frequencies of C to T and G to A transitions at the 5′ and 3′ end of DNA fragments respectively. Plot created with PMDtools.
Chapter 17
1. Figure 17.1 Map showing the approximate locations of the 56 cranial samples used in the example. This is a modified version of a figure used in Pietrusewsky (2008a) with permission of Etty Indriati, Gadjah Mada University, Yogyakarta, Indonesia.
2. Figure 17.2 Plot of 56 group means on the first two canonical variates after applying stepwise discriminant function analysis to 27 cranial measurements. Abbreviations of the cranial samples are explained in Table 17.1. This is a modified version of a figure used in Pietrusewsky (2008a) with permission of Etty Indriati, Gadjah Mada University, Yogyakarta, Indonesia.
3. Figure 17.3 Plot of 56 group means on the first three canonical variates after applying stepwise discriminant function analysis to 27 cranial measurements. Abbreviations are explained in Table 17.1. This is a modified version of a figure used in Pietrusewsky (2008a) with permission of Etty Indriati, Gadjah Mada University, Yogyakarta, Indonesia.
4. Figure 17.4 Dendrogram (or diagram of relationship) that results from applying the UPGMA clustering algorithm to Mahalanobis distances using 27 cranial measurements recorded in 56 male groups. This is a modified version of a figure used in Pietrusewsky (2008a) with permission of Etty Indriati, Gadjah Mada University, Yogyakarta, Indonesia.
Chapter 18
1. Figure 18.1 The effects of population increase or decrease on estimates of the age‐at‐death distribution and age‐specific survival (the probability of surviving from birth to each subsequent age) are shown. The upper graph gives the distribution of ages at death in five stable populations with identical age‐specific mortality rates but different growth rates (r). Age‐specific mortality rates are generated by a mixed Makeham model (O’Connor et al. 1997; Wood et al. 2002) with parameter values α₁ = 0.5, α₂ = 0.0005, α₃ = 0.005, β₃ = 0.05, and ρ₀ = 0.1. In the lower graph, age‐specific survival is estimated from the same age‐at‐death distributions under the erroneous assumption that all five populations are not only stable but stationary (r = 0). Positive growth makes it appear as if survival is lower at each age, whereas negative growth has the opposite effect.
2. Figure 18.2 A simple model of heterogeneous frailty and selective mortality is shown here for a cohort of newborns one and two months old. Each child’s risk of dying is constant and proportional to its individual‐level frailty. Frailty is assumed to be distributed as a gamma random variable among newborns, as shown in the top graph, with the right tail being the riskiest place to be. Deaths during the first month (dots) are selective with respect to the frailty distribution, so children of high frailty make up a disproportionately large fraction of all deaths. The frailty distribution, therefore, shifts downward by the second month of life, as shown in the bottom graph (compare solid and dashed lines), as does the mean frailty, indicated by an arrow. The aggregate‐level hazard of death at each age is proportional to the mean frailty of survivors at that age, so the aggregate hazard declines even though the hazards of the individual children remain constant.