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 The Bioarchaeology of
Metabolic Bone Disease
 The Bioarchaeology of
Metabolic Bone Disease
Second Edition

Megan B. Brickley is currently Tier One Canada

Research Chair in the Bioarchaeology of Human Disease,
based in the Department of Anthropology, McMaster University,
ON, Canada

Rachel Ives is currently Curator of Anthropology,

Natural History Museum London, United Kingdom

Simon Mays is currently Human Skeletal Biologist for

Historic England, based in Portsmouth, United Kingdom (UK).
He is also a Visiting Lecturer at the Department of Archaeology,
University of Southampton, UK and a Honorary Fellow at the School of
History, Classics and Archaeology, University of Edinburgh, UK
Academic Press is an imprint of Elsevier
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Dedication

Megan Brickley would like to dedicate this book to Beatrice, the excellent cat from Barton
Street, Hamilton, ON, Canada.
6 February 2011 21 October 2019.
Contents

Preface xi

Acknowledgements xiii

1. Introduction to the study of metabolic bone diseases 1

2. The study of metabolic bone disease in bioarchaeology 5

Approaches to the study of metabolic bone disease 5
Diagnosis of metabolic bone disease in palaeopathology 7
Core concepts 22

3. Biology and metabolism of mineralised tissues 23

Bone structure 23
Bone formation and bone growth 30
Dental tissues 38
Osteoimmunology 38
Core concepts 40

4. Vitamin C deficiency, scurvy 43

Scurvy today, epidemiology and current views on aetiology 43
The biology of skeletal changes 46
Diagnosis of scurvy in skeletal remains 52
Palaeopathology of scurvy 68
Anthropological perspectives 72
Core concepts 74

vii
viii Contents

5. Vitamin D deficiency 75
Vitamin D deficiency today, epidemiology, and current views on
aetiology 75
The biology of changes in mineralised tissues 91
Diagnosis of vitamin D deficiency in skeletal remains 95
Palaeopathology of rickets, residual rickets, and osteomalacia 121
Core concepts 127

6. Age-related bone loss and osteoporosis 129

Osteoporosis today, epidemiology, and current views on
aetiology 130
The biology of skeletal changes and complications 136
Diagnosis of age-related osteoporosis in skeletal remains 144
Palaeopathology of osteoporosis 157
Anthropological perspectives 160
Core concepts 163

7. Secondary osteoporosis 165

Secondary osteoporosis today, epidemiology, and current views on
aetiology 165
The biology of skeletal changes and complications 167
Diagnosis of secondary osteoporosis in skeletal remains 170
Palaeopathology of secondary osteoporosis 171
Core concepts 178

8. Paget’s disease of bone 179

Paget’s disease of bone today, epidemiology, and current views on
aetiology 179
The biology of skeletal changes 181
Diagnosis of Paget’s disease of bone in skeletal remains 185
Palaeopathological cases of Paget’s disease of bone 193
Anthropological perspectives 197
Core concepts 199
 Contents ix

9. Anaemia 201
Anaemia today, epidemiology, and current views on aetiology 201
The biology of skeletal changes and complications 208
Diagnosis of anaemia in skeletal remains 211
Palaeopathology of anaemia 222
Core concepts 224

10. Disease co-occurrence 227

The biology of skeletal changes and complications in co-occurring
conditions 229
Palaeopathology of co-occurrence 239
Core concepts 247

11. Overview and directions for future research 249

Palaeopathological diagnosis 249
Integration of palaeopathology with historical sources 252
Integration of palaeopathology with theoretical approaches 253
Increasing the relevance of metabolic bone diseases to public health
and modern medicine 254
Final thoughts 254

References 257

Index 305
Preface
The 12 years since the appearance of the first edition of this book have been a period of
intense research that has resulted in significant advances in the diagnosis and interpretation
of metabolic bone disease in skeletal remains. Because of the importance of recent work,
this new edition has been comprehensively updated. The book has also acquired an addi-
tional author, Simon Mays; this has broadened the perspectives provided, adding to the
range of coverage. In our updates, we have revised every chapter, made some alterations in
emphasis and approach, and have also added two completely new chapters.
The late Don Ortner was kind enough to provide a positive and enthusiastic Foreword for
the first edition. He was a key researcher in the bioarchaeology of the metabolic bone dis-
eases. Some of the approaches and perspectives he pioneered have been key to informing
the revisions we have made for this edition. Don stressed that approaches to palaeopathol-
ogy needed to avoid being overly simplistic, and his later work emphasised the importance
of developing a good understanding of the pathophysiology of bone lesions for the correct
diagnosis and interpretation of disease in skeletal remains. He particularly applied this per-
spective to the diagnosis of some of the metabolic bone diseases. Throughout this edition,
we emphasise and further develop this ‘biological’ approach, stressing the links between the
alterations to bone metabolism wrought by the various conditions and the lesions produced
in the skeleton.
The first of the two new chapters in this edition deals with anaemia. When writing the
first edition, anaemia was not thought to affect the actions of bone cells (links between bone
marrow and bone cells were still being established) and was not included in the classical
clinical and palaeopathological texts on the metabolic bone diseases. These points were
seized on by Megan Brickley as reasons not to include it. The opening slide of Megan’s class
on anaemia in palaeopathology has always featured a photograph of a dung heap, and this
summed up her feelings on the topic. Don was disappointed that anaemia was not covered
in our first edition. He reasoned that, because the most common cause is micronutrient defi-
ciency, in common with some of the other metabolic bone diseases, inclusion provides
important additional information on conditions with a nutritional component. Mindful of
this, and of the importance of developing a biological understanding of the basis for skeletal
lesions of anaemia if this condition is to be distinguished from other metabolic bone diseases
that may produce similar skeletal lesions, we now include a chapter devoted to it.
The other new chapter deals with co-occurrence of disease. This was another theme close
to Don’s heart, which he often summed up in the aphorism ‘a dog may have both ticks and
fleas’. Co-occurrence is a particularly important topic in the context of the metabolic bone
diseases. Some of these conditions share risk factors in common, and medico-historical
sources confirm that some of the diseases considered in this book regularly co-occurred in

xi
xii Preface

individuals in the past. In addition, the presence of one condition may modify the manifesta-
tion of another, which poses particular difficulties in palaeopathological diagnosis. These are
among the considerations that prompted us to provide coverage of this topic.
This fully updated edition reflects the significant advances that have been made in
palaeopathological diagnosis and interpretation of metabolic bone disease in the past. We
hope that the new perspectives described in this book will further confirm the study of meta-
bolic bone disease as a key area of palaeopathological enquiry and will act as a basis for con-
tinued progress in the future.

Megan Brickley, Rachel Ives, Simon Mays

 1
Introduction to the study
of metabolic bone diseases
The Bioarchaeology of Metabolic Bone Disease, Second Edition, covers deficiencies of vitamin
C and D, age-related bone loss and osteoporosis, other causes of bone loss, and Paget’s dis-
ease of bone (PDB); all the conditions covered in the first edition and certain other condi-
tions arising from imbalances of bone metabolism. This edition also includes two important
new chapters, the first covering anaemia and the second focusing on the co-occurrence of
disease. Metabolic bone diseases constitute a significant impediment to health in a global
context today. Anaemia is the most widespread condition in the world, with an estimated
quarter of the global population being affected by some form of this condition (Pasricha
et al., 2013), and over a billion people are estimated to be vitamin D deficient, with cases of
rickets suggested to be on the rise (Robinowitz, 2009; Elder and Bishop, 2014). Worldwide
fractures associated with age-related bone loss and osteoporosis affect an estimated 8.9 mil-
lion individuals annually (Kanis et al., 2017), contributing significantly to morbidity and mor-
tality. Amongst groups with European ancestry, PDB is the second commonest disease of
bone after osteoporosis (Tuck et al., 2017). Although cases of scurvy are rare in most con-
texts, sub-clinical and clinical vitamin C deficiencies are widespread (Akikusa et al., 2003),
with cases of scurvy found in a number of vulnerable groups and during times of conflict
and natural disasters (Cheung et al., 2003; Lux-Battistelli and Battistelli, 2017). The impor-
tance of many conditions on bone has increasingly been recognised, and recent develop-
ments have also highlighted the effect on bone of conditions in the metabolic syndrome, a
group of conditions that is seeing an exponential rise around the globe (Grundy, 2008;
Jiamsripong et al., 2008). Moreover, clinical medicine is recognising the importance of
co-occurrence of conditions and the complex factors involved in co-occurrence of disease,
particularly those linked to micro-nutrient (Klimek et al., 2016; Bharati et al., 2018). There is
also increased recognition of early life events contributing to the development of many of
these conditions (Lockau and Atkinson, 2018).
With intricate links to social, biological, and environmental factors, understanding the
metabolic bone diseases offers an unparalleled means of gaining better insights into past
communities and a deeper appreciation of humanity in the broadest sense, fundamental
areas for bioarchaeologists and anthropologists more widely. Understanding disease pres-
ence and prevalence in past communities provides fuller information enabling us to get bet-
ter insights into life and death for those individuals, many of whom were silent even in the
limited part of human existence with written records. Critically, an understanding of the

The Bioarchaeology of Metabolic Bone Disease. DOI: https://doi.org/10.1016/B978-0-08-101020-4.00001-X

© 2020 Elsevier Ltd. All rights reserved.
1
2 The Bioarchaeology of Metabolic Bone Disease

time-depth of health problems also provides an important new dimension to comprehending

current public health issues. Looking back enables a more perceptive view of the future.
“Metabolic bone diseases are conditions that cause an alteration in normal bone forma-
tion, resorption, or mineralisation, or a combination of these; in most conditions these
alterations are systemic” (Brickley and Mays, 2019: 531). Many of the metabolic bone dis-
eases arise as a direct result of nutritional deficiency, as in the case of vitamin C deficiency
(scurvy) or vitamin D deficiency (rickets and osteomalacia), or are intricately linked to defi-
ciencies of micro-nutrient such as iron, folate, and vitamin B12 (as is in many acquired anae-
mias). Nutritional quality also plays a role in acquisition of peak bone mass and so,
alongside hormonal changes, will be critical in the development of age-related bone loss and
osteoporosis. The aetiological mechanisms involved in the development of other conditions
covered, such as PDB, are less clearly understood, but all have intricate links between bone
cell activity and lesion manifestation in mineralised tissues. Placing a biological approach to
palaeopathological diagnosis (Mays, 2018a) at its core to supplement information obtained
through comparison to clinical and biomedical reports, this book explores the bioarchaeol-
ogy of this group of conditions.
The importance of using wider contextual information, a critical part of bioarchaeology, is
integrated throughout the text, and we highlight how an integrated appreciation of the meta-
bolic bone diseases within many modern cultures can broaden the interpretative frameworks
considered. We have drawn on the extensive recent research into the characteristics of these
diseases in modern populations. The chapters of this book provide a framework with which
to consider the conditions covered, enabling readers at all career stages to integrate informa-
tion and approaches into future research projects.
Each chapter provides a clear synthesis of current knowledge on the condition/s covered.
An emphasis is placed on the biology of skeletal changes; basic biological mechanisms
underlying the disease process are set out, and, as appropriate, approaches to diagnosis in
palaeopathology using macroscopic, radiographic, and histological/micro-CT analysis
grounded in up-to-date understanding of the disease are provided. Terms used in the text
are explained, and many new illustrations are used to set out information useful for those
with a variety of previous experience to build their skill base in consideration of conditions,
whether based in an academic, commercial, or museum/public office setting. A discussion
of palaeopathological cases of the conditions that highlight approaches to diagnosis is pro-
vided. Population level studies can be used to elicit information on the use of the presence
of these conditions to increase our understanding of environmental stress and social and cul-
tural factors operating in past groups, and examples are provided.
Many chapters contain a section on Anthropological Perspectives, designed to illus-
trate how the analysis of the metabolic bone diseases can provide insights into issues
considered by the broader anthropological community. The Boxes contained in many
chapters explore a range of key concepts which could be investigated by considering dis-
ease interactions, modern versus past perspectives, texts versus skeletal evidence, or ani-
mal versus human disease expression, in order to enhance the study of bioarchaeology.
 Chapter 1 • Introduction to the study of metabolic bone diseases 3

Chapter 2, The study of metabolic disease in bioarchaeology, introduces the study of

these conditions and highlights the benefits and challenges of the sources and approaches
that are available to enable investigation of these diseases in the past. The importance of
understanding the biological mechanisms underlying disease processes is set out and a clear
guide to taking a biological approach to diagnosis is provided. Uses of clinical and biomedi-
cal data are reviewed, and this chapter outlines the wider relationship that bioarchaeological
research has with investigations within the many sub-disciplines of anthropology, most
critically palaeopathology.
Accurate interpretations of the metabolic bone diseases are enhanced by recogni-
tion of both the normal and pathological processes evident at the bone cellular level.
Chapter 3, Biology and metabolism of mineralised tissues, presents an introduction to
the processes that underpin understanding of the conditions covered. The other criti-
cal factors that underlie lesion formation, mechanisms inherent in bone growth
(modelling) and maintenance (remodelling), as well as the functions of individual cells
and the systemic and local factors that can influence cell behaviour, are reviewed. We
take a commonly occurring skeletal lesion, porotic bone, and illustrate the four basic
biological mechanisms that can result in the formation of this lesion type. In combina-
tion with the approach to diagnosis set out in Chapter 2, this provides a tool kit
that can be applied to all conditions covered, facilitating integration of material into
projects of all types.
The subsequent chapters of this book each discuss a specific metabolic bone disease,
considering the nature of the disease process and aetiology for vitamin C deficiency (scurvy),
vitamin D deficiency (rickets and osteomalacia), age-related bone loss and osteoporosis, sec-
ondary bone loss, Paget’s disease of bone, and anaemia. Disease co-occurrence is considered
in Chapter 10, alongside conditions in the metabolic syndrome. In Chapter 10 information
presented in the dedicated chapters on conditions are drawn on to demonstrate how recog-
nition and understanding of factors that can influence the development of disease co-
occurrence have implications for considering the manifestations of lesions in mineralised tis-
sues. The effect of conditions that do not produce diagnostic lesions on bone remodelling
are considered, and we emphasise the need for wider consideration of these issues in
bioarchaeology and palaeopathology.
The final chapter of the book, Chapter 11 Overview and future directions for research,
draws together the principal findings and concepts covered in the book; a summary of areas
of future research is provided. This chapter provides a reference for those who wish to dis-
cover the fields in which future research on these subjects might most fruitfully be directed.
Ultimately, the range of information brought together in this book aims to demonstrate that
the metabolic bone diseases have an increasingly important role to play in bioarchaeology
and the wider discipline of anthropology through enabling a fuller understanding of health
and its complex interactions in past human life.
Throughout the book we have endeavoured to expand these insights to develop under-
standing of this important group of conditions, giving updated information for those
4 The Bioarchaeology of Metabolic Bone Disease

who have been working in the field for a while and offering a structured framework for those
new to the field. As set out at the start of the chapter, the conditions covered in this book are
critically important to today’s community and are likely to have fundamentally shaped those
of our ancestors. Insights provided through bioarchaeological research have a critical role to
play in increasing our understanding of both past and present communities.
 2
The study of metabolic bone
disease in bioarchaeology
The study of metabolic bone disease has an important role to play in improving the under-
standing of life in both past and present societies, and information on these conditions is
assuming an increasingly significant role in many branches of anthropology. When consid-
ered at the population level, data on prevalence of these conditions will, amongst other
areas, broaden understandings of subsistence strategies, living and environmental condi-
tions, migration and adaptation, social and cultural practices, and marginalised living, as
well as the effects of childhood growth and the ageing process. We have utilised a range of
evidence that contributes to the investigation of metabolic bone disease in mineralised tis-
sues, providing examples demonstrating how improved understanding of these conditions
benefits work undertaken in bioarchaeology and palaeopathology, and have highlighted
some of the contributions to wider anthropological debates. We have also illustrated how
theoretical approaches have the potential to maximise interpretations of disease manifesta-
tions and considerations of changing palaeoepidemiological, geographical and temporal
trends of disease presence. In this chapter, the key sources of evidence and approaches
available to those investigating the metabolic bone diseases in bioarchaeology and palaeo-
pathology are outlined and the potential and limitations considered.

Approaches to the study of metabolic bone disease

A bioarchaeological approach to the study of metabolic bone disease enables a range of the-
oretical approaches to be taken to obtain the maximum amount of information from the
palaeopathological study of human remains. Recent syntheses (e.g. Grauer, 2012, 2018) have
argued that studies based purely on palaeopathology have tended to lack strong theoretical
components. Clear diagnostic frameworks (e.g. Mays, 2018a) and solid recording and
description of lesions (Klaus, 2017) are fundamental elements in the study of metabolic bone
diseases, and biological processes in these conditions sit at the core of this book. However, a
more meaningful understanding of palaeopathological evidence will be obtained if elements
of archaeological theory are also incorporated (Grauer, 2012).
Bio-cultural approaches, in which biological information is considered as interacting with
the cultural context (Dufour, 2006; Zuckerman and Armelagos, 2011), have been successfully
integrated into the work of bioarchaeologists for many years; examples of investigations using
such approaches are included throughout the book. More recently, aspects of a life course
approach have also been integrated into bioarchaeological work. A life course approach is the
The Bioarchaeology of Metabolic Bone Disease. DOI: https://doi.org/10.1016/B978-0-08-101020-4.00002-1
© 2020 Elsevier Ltd. All rights reserved.
5
6 The Bioarchaeology of Metabolic Bone Disease

recognition that the transition through life is culturally constructed, and the life course itself
may vary depending on status and sex, together with the surrounding constraints of the com-
munity or society (Agarwal, 2016). This type of approach has been adopted by scholars work-
ing in ancient history and archaeology investigating various contexts (e.g. Harlow and
Laurence, 2002; Gilchrist, 2012). Bioarchaeological investigations invariably involve analysis of
individuals that have reached the end of their lives, but aspects of the life course approach
can be integrated into such studies, and palaeopathological investigations of metabolic bone
diseases offer a particularly valuable source of information (e.g. see Lockau et al., 2019).
Childhood in particular is both a biological phenomenon and a social construct, with huge
differences observed between societies (Lewis, 2007:1 13; Halcrow and Tayles, 2008). Within
the biological interpretation of the life course, culturally and behaviourally mediated influ-
ences on life and health will be inherently inter-linked with the surrounding environment and
dietary practices (e.g. see Chapter 4: Vitamin C deficiency, scurvy). However, both factors may
further vary depending on the position of the individual in the community. Such interactions
may be reflected in the expression of metabolic bone diseases within a society. For example,
possible changes in clothing types as individuals aged, or varying attitudes towards exposure
of skin and slight changes in synthesis with age, may link vitamin D deficiency to both biologi-
cal and social phenomena (see Chapter 5: Vitamin D deficiency).
In many cultures, the critical years of infancy and childhood are those during which there
is the greatest risk of potentially fatal disease; in past communities, individuals that survived
this period had a reasonable chance of living into older age (e.g. Thane, 2000; Blurton Jones
et al., 2002). Bioarchaeological research is developing approaches to investigate the experi-
ences of ageing in the past (e.g. Borkan et al., 1982; Cave and Oxenham, 2016; Gowland, 2016;
Appleby, 2018). At later stages of the life course, the onset of the menopause, which has clear
links to the development of conditions such as age-related bone loss and osteoporosis, may
have marked a new stage in the life course of women. There needs to be greater awareness of
the effects of ageing on disease processes, and the extent to which males and females might
be differently affected (Chapter 6: Age-related bone loss and osteoporosis). Factors that may
affect the development of metabolic bone diseases are presented in Fig. 2 1.

FIGURE 2–1 Schematic relationship of some of the key factors that may affect and interact in the development of
metabolic bone diseases. The position of the various factors included in each section does not denote importance.
 Chapter 2 • The study of metabolic bone disease in bioarchaeology 7

Sometimes it will be possible to determine if lesions indicate a disease active at the time
of death, such as the presence of a cutting cone in a long bone of an individual with Paget’s
disease of bone (PDB, see Chapter 8: Paget’s disease of bone), or else represent residua of
earlier, healed episodes, as in the case of residual rickets (see Chapter 5: Vitamin D defi-
ciency). Increased consideration of the stage of disease represented by lesions is likely to
feed into the contribution that bioarchaeologists can make to investigations employing para-
digms such as the Developmental Origins of Health and Disease hypothesis (Gowland,
2015). Biomedical research has indicated strong links between the long-term ability to attain
peak bone mass and early life experience of metabolic bone diseases (Sanz-Salvador et al.,
2014; Chapter 6: Age-related bone loss and osteoporosis), and between in utero vitamin D
deficiency and later susceptibility to conditions in the metabolic syndrome (Belenchia et al.,
2017) (see Chapter 10: Disease co-occurrence). Many of the conditions covered in this book
can manifest at any stage of an individual’s life with recurrent episodes, and use of the life
course approach was recently discussed by Brickley et al. (2014) in relation to vitamin D defi-
ciency. More recently new approaches, such as discussing the lived experience and consider-
ing the bioarchaeology of care, have started to be applied. These approaches are not specific
to particular conditions, but the bioarchaeology of care is considered here in Chapter 7,
Secondary osteoporosis, and the lived experience in Chapter 8, Paget’s disease of bone.

Diagnosis of metabolic bone disease in palaeopathology

In palaeopathology, most diagnoses are made on the basis of the morphology of skeletal
lesions and their distribution in the skeleton. The main conceptual approach in lesion-based
palaeopathology is comparative (Mays, 2018a:13; see also Grauer, 2018). Lesions in a refer-
ence group are used to help us to make a diagnosis in a target skeleton using the lesions
that are present. The target skeleton is our archaeological individual. Reference samples
comprise cases where there is independent evidence concerning which disease an individual
was suffering from. An important type of reference material in palaeopathology is human
remains kept in medical museums and other institutions, taken from those whose disease
was diagnosed in life or at autopsy. Another is radiographic or other skeletal imaging studies
of living individuals.
Although the comparative approach has clear strengths, anchoring our diagnosis to
known cases of disease, it also has significant weaknesses (Mays, 2018a). Human remains
held by medical pathology museums provide a biased and incomplete record of the effects
of disease on the skeleton. In most cases, collections were amassed in the 19th and early
20th centuries, and often there was a bias towards the spectacular or the unusual. For exam-
ple cases in pathology museums with diagnoses of vitamin C or vitamin D deficiency tend to
show much more severe bony changes than will usually be encountered archaeologically
(see Ives and Brickley, 2014). Unless lesions were considered important for illustrating a dis-
ease, material exhibiting these changes was unlikely to have been incorporated into collec-
tions. In addition, prior to modern medical protocols for evaluating disease, clinicians would
8 The Bioarchaeology of Metabolic Bone Disease

have been unaware of the full gamut of skeletal lesions produced by a disease (Weston,
2008; Mays, 2012). For example as we shall see in Chapter 4, Vitamin C deficiency, scurvy,
work by Don Ortner has established that porosity of the sphenoid bone is an important skel-
etal sign of scurvy, but this alteration does not feature in skeletal pathology held in medical
museums. Many bones harvested for pathology museum collections may have come from
individuals with multiple conditions, but museum catalogues often only have one condition
recorded. For example infantile scurvy and rickets often co-occurred (see Chapter 10:
Disease co-occurrence), and some pathology museum examples labelled as showing one of
these diseases appear also to show lesions due to the other (see Fig. 2 2).
There are also some difficulties associated with using medical imaging data on living
patients as a baseline. First, most images are plain film radiographs. An alteration in radioden-
sity of at least 40% is needed for a bone change to show on a radiograph (Ortner, 1991). This
means that many alterations that are clearly evident on dry bone are invisible radiographically
for example this would be the case for many of the porous/new bone formation lesions we
describe in Chapter 4, Vitamin C deficiency, scurvy. Second, images are only taken in living
patients when there is a clear clinical need. For example diagnosis of scurvy in clinical practice
is made based on signs and symptoms shown by the patient, and the condition responds

FIGURE 2–2 Cranium of a 2-year-old child held in the Federal Museum of Pathological Anatomy, Vienna. This
cranium is recorded as being from a child with a ‘rachitis cranium’, but porosity on the sphenoid and other changes
across the cranium indicate that this child may also have been deficient in vitamin C. The co-occurrence of rickets
and scurvy is discussed in more detail in Chapter 10, Disease co-occurrence. Photograph by the authors, courtesy of
the Federal Museum of Pathological Anatomy, Vienna.
 Chapter 2 • The study of metabolic bone disease in bioarchaeology 9

readily to administration of vitamin C (Agarwal et al., 2015). Imaging of the skeleton for
lesions is unnecessary for diagnosis or treatment and so is not normally undertaken.
It is increasingly being recognised that the traditional comparative approach to diagnosis
needs to be supplemented by the so-called biological approach. This involves building up a
biological understanding of the response of the skeleton to various diseases, so that we are
more able to understand (and hopefully correctly interpret) the lesions we observe in archae-
ological bones and dental material. In part, the need for this approach arises from shortcom-
ings, of the types discussed above, in our reference material. However, diagnosis in
palaeopathology should always be more than a pattern-matching exercise between reference
and target material. Different diseases may produce fairly similar lesions in the skeleton. A
good biological understanding may help us to tease out subtle differences in lesions caused
by various disease processes, such as differences in morphology of porous alterations due to
haemorrhage in scurvy from those due to poor mineralisation of growing surfaces in rickets
(see Chapter 5: Vitamin D deficiency). Not only may different diseases produce similar
alterations, but, in a given disease, bone lesions may vary due to factors including the length
of time the individual had the disease, whether the disease was active or quiescent at time of
death, and the nutritional status of the person. We are in a better position to understand the
potential influences of these factors on lesion morphology and distribution if we have a
clearer understanding of the biological processes that lead to lesion formation.
The biological approach has been key in developing diagnostic criteria for some meta-
bolic conditions in palaeopathology. Because of this, in this book we use both documented
reference cases and also archaeological material to illustrate pathology typical of various
metabolic bone diseases. A biological approach to lesion evaluation may involve the follow-
ing (Klaus, 2017):
• Observe the morphology of each lesion (see Chapter 3: Biology and metabolism of
mineralised tissues and Fig. 3 6)
• Evaluate the lesion type found at each location
• Consider the anatomical distribution of lesions
• In the absence of previous detailed readings of the biomedical literature, or availability of
new information, review the biomedical literature
• Pay close attention to relationships between hard and soft tissue anatomical structures at
the sites in the skeleton where lesions were characteristically seen
• Systematically evaluate data gathered to determine the conditions that could have
produced each lesion and the probability of the various diagnoses considered
• Consider basic biological information (age, sex, ancestry) and completeness and
preservation of the individual under assessment
• Remember lesions observed don’t necessarily reflect a single disease, or conditions that
were active simultaneously, or at the time of death (see Chapter 10: Disease co-
occurrence).
The conditions discussed in this book generally cause a diverse array of changes in the
skeleton. Usually, no particular lesion is pathognomonic (i.e. enables diagnostic certainty). In
10 The Bioarchaeology of Metabolic Bone Disease

addition, the variability in the potential expression of different disease conditions means that
it is not possible to provide categorical statements on the number of lesions that must be
present in order to make a diagnosis. Individual judgement rather than an algorithmic
approach involving counting of lesions is required in palaeopathological diagnosis. This
might seem a bit subjective, but professional judgement plays a central role in clinical diag-
nosis, and evidence is emerging from cognitive sciences that judgement may sometimes
result in more accurate decision-making than do complex scoring procedures (Mays, 2018a).
For one condition discussed in this book, osteoporosis (see Chapter 6: Age-related bone
loss and osteoporosis and Chapter 7: Secondary osteoporosis), we are largely forced to step
away from a lesion-based approach to diagnosis. Osteoporosis is characterised by loss of
bone mass and micro-structural deterioration without producing characteristic gross skeletal
lesions. In palaeopathology, osteoporosis is normally evaluated using quantitative measures
of bone mass or micro-structural integrity. The aim is normally not to identify individuals
suffering from osteoporosis (although this can be done) but to study bone mass or micro-
structural integrity as a continuous, quantitative variable. In this way, loss of bone mass or
integrity with advancing age or after injury can be quantified and compared between differ-
ent populations or between different sub-groups within a population. Its effects on health
can also be studied by evaluating relationships between these parameters and fracture. For
investigations of osteoporosis associated with age-related bone loss, this presupposes
a population-based approach rather than one that concentrates on diagnosis in individual
cases.

Collections of human and animal remains

In addition to the pathology museum collections that have been discussed, there are a range
of collections of fossil, and more recent, human and animal skeletal and dental material held
at institutions around the world. A number of the collections consist of documented human
remains, and well-known examples include those curated at universities and museums such
as Lisbon (Cardoso, 2006) and Coimbra in Portugal (Cunha and Wasterlain, 2007), the
Robert J. Terry anatomical collection held at the Smithsonian Institution's National Museum
of Natural History, in Washington DC, USA (Hunt and Albanese, 2004) and the W.M. Bass
donated skeletal collection held at the University of Tennessee, Knoxville, USA (Vidoli et al.,
2017). Most work using such collections involves development of techniques that contribute
to building the biological profile of individuals (e.g. age-at-death, sex, ancestry). Work has,
however, also been undertaken on metabolic bone diseases. Data on the sex and age-at-
death of individuals and co-occurrence of disease has enabled conditions such as age-
related bone loss to be explored (see Chapter 6: Age-related bone loss and osteoporosis).
Information on aspects of life and circumstances of death has contributed to research on
osteoporosis and osteomalacia in the Hamann-Todd collection (Mensforth and Latimer,
1989; Mensforth, 2002). Recently, issues linked to the metabolic syndrome, such as estima-
tion of BMI and obesity from skeletal remains, have started to be tackled (e.g. Harrington
and Wescott, 2015; Wheeler et al., 2015). The background of individuals represented in such
 Chapter 2 • The study of metabolic bone disease in bioarchaeology 11

collections, however, has considerable implications for the reflections of the pattern of dis-
eases represented (de la Cova, 2010) and should be considered further in future research
(see Chapter 10: Disease co-occurrence).
There are also examples of animals with evidence of metabolic bone disease in museum
collections (e.g. DeGusta, 2010; Farrell et al., 2015). Detailed analysis of mummified baboons
from Ancient Egypt that were kept in captivity, for example revealed cases of rickets
(Chapter 5: Vitamin D deficiency) and scurvy (Chapter 4: Vitamin C deficiency, scurvy)
(Nerlich et al., 1993). Investigations of metabolic bone disease in non-human animals pro-
vide a valuable additional source of data that can provide fresh insights into the development
of these conditions (see Chapter 5: Vitamin D deficiency and Chapter 6: Age-related bone
loss and osteoporosis).

Clinical and biomedical data

Clinical and biomedical data provide an important set of reference material and were foun-
dational in palaeopathology and later bioarchaeological research. Clinical data are not, how-
ever, without complications. There is, for example notable variation in terminology applied
to the skeletal manifestations, and diagnoses, of disease by clinicians, and a lack of standar-
disation is touched on in a number of conditions covered in this book. Within clinical medi-
cine there has also been greater appreciation of the number of cases of misdiagnosis,
something those working with less evidence in palaeopathology would do well to consider.
This shift is probably a result of much wider use of biomedical tests, not because there has
been an explosion of numbers of people with these conditions. Recent sharp increases in
clinically reported cases of co-occurring disease have occurred as clinicians, like palaeo-
pathologists, have started to recognise that disease co-occurrence is common and is impor-
tant for properly understanding what is happening in a patient (see discussion in
Chapter 10: Disease co-occurrence).
Bone cell activity lies at the basis of understanding and recognising the metabolic bone
diseases in both modern and past populations. There is now considerable evidence from
experimental studies in cell biology, clinical trials investigating new treatments, reviews of
disease epidemiology, case studies reporting specific manifestations of a condition, and ran-
domised large-scale population surveys of specific health indicators. Significant develop-
ments have taken place in the understanding of clinical skeletal biology over the past 12
years, and these clinical and biomedical sources all offer relevant information, but the poten-
tial and limitations of each for palaeopathology need recognition (e.g. see Lockau and
Atkinson, 2018). As emphasised throughout this book, an integrated understanding of bone
biology and skeletal responses to various conditions is vitally important for understanding
health in past populations (see also Gosman, 2012b; Ragsdale and Lehmer, 2012), but this
work can be complex to interpret and does not always translate into proven causative links
in human models. Similarly, disease outcomes reported from clinical trials may not be
reflected in randomised large-scale population studies.
12 The Bioarchaeology of Metabolic Bone Disease

Archaeological human remains

Human remains excavated from archaeological sites allow investigations of the extent of
metabolic bone diseases through time and across a variety of settings (e.g. see Brickley et al.,
2017 discussing vitamin D deficiency). For communities without written texts, the study of
human remains is the primary source of evidence relating to metabolic bone diseases. In
many respects, direct analysis of human skeletal remains is no less important when written
sources of information are available. Extraction and interpretation of information from texts
is rarely simple (see Mitchell, 2011, 2017; Mays, 2018a); Box 2 1 sets out the value of this
form of evidence for learning about metabolic bone disease. Many archaeological human
remains can be directly associated with a particular cultural or social group, and contextual
information can add significantly to the interpretation made. Factors such as grave construc-
tion have been used as a proxy for status through evaluation of level of resources mobilised
(Keegan, 2002; Goldstein, 2006). Goods deposited with deceased individuals are complex to
interpret, but can assist in the assessment of life stage and gender (Hollimon, 2011; Newman
and Gowland, 2017) (Fig. 2 3).
The distribution of cases of a condition can be a reflection of archaeological excavation
activity (Mays, 2010). Over the last two decades, with re-development of many urban centres
in North America, Europe and Oceania, increasing numbers of individuals buried in the 18th
and 19th centuries have been excavated and analysed. Examples include St. Thomas’
Anglican Church, Belleville, Ontario (Saunders et al., 2002), St. Martin’s, Birmingham,
England (Brickley et al., 2006), and more recently what were formally rural Dutch (Veselka
et al., 2015) and suburban 19th century British sites (Watts and Valme, 2018). Investigations
are also now underway on collections of this date from Australia and New Zealand. At some
such sites there is considerable detail available, including individual identity and documen-
ted cause of death (see Molleson and Cox, 1993; Ives, 2015).
Factors relating to formation of collections need to be taken into consideration in evaluat-
ing evidence from archaeological human remains and interpretation of results.
Consideration should be given to the way in which a skeletal assemblage, excavated from an
archaeological site and curated at an institution, represents a once living community
(Waldron, 1994; Boldsen and Milner, 2012). Variables that contribute to determining the evi-
dence available include which individuals die at different ages, who is buried, and who has
body parts that survive, are excavated, and then curated. Taphonomic factors such as soil
acidity, moisture levels and temperature may affect the preservation of bones. Preservation
and survival of human bone from archaeological sites have been dealt with by various
authors (e.g. Waldron, 1987; Mays, 1992; Stojanowski et al., 2002). Lyman (1994) reviewed
many aspects of vertebrate taphonomy, but this is still a poorly understood area. Size of skel-
etal elements does, however, appear to play a role in their recovery from archaeological sites
(Mays, 1992; Adams and Konigsberg, 2008); at a basic level, it appears that smaller bones
survive less well, and bones with higher trabecular bone content are also prone to loss.
As was demonstrated at St. Martin’s, Birmingham, England, the decision to concentrate the
available resources on the better preserved, more complete skeletons (Brickley et al., 2006)
 Chapter 2 • The study of metabolic bone disease in bioarchaeology 13

BOX 2 1 The value of written sources for the bioarchaeology of metabolic bone disease

Among the conditions discussed in this book, Paget’s disease of bone was only described in 1877,
and until Roentgen discovered X-rays in 1895 there was no way of assessing loss of bone density in
osteoporosis. Written sources can therefore contribute little to our understanding of these diseases
in ancient populations. Scurvy and rickets were recognised in Classical Antiquity, but documentary
sources on these conditions only become plentiful from the 18th century AD onwards in Europe.
Bioarchaeologists are generally interested in patterning in disease at a population level. In assessing
the value of written sources for our understanding of scurvy and rickets, a key question is the extent
to which they can contribute to our knowledge of prevalences of these diseases in 18th and 19th
century populations.
Many early European documentary sources on scurvy deal with the disease in military,
particularly naval, personnel. This was because, in the 18th and 19th centuries, the power of the
great mercantile nations of Western Europe was underpinned by naval power. A disease, such as
scurvy, that threatened the efficiency of navies had serious consequences, so there was every
incentive to try and understand the condition and hence develop ways of combatting it. By
contrast, there is little on scurvy in civilian populations until the closing decades of the 19th
century, when infantile disease began to be noted as a problem connected with the use of milk
sterilised by heating (Carpenter, 1986:158-172).
For civilian populations, we have many more sources on rickets than on scurvy (Mays, 2018b).
From the 18th century onwards, as the problem of rickets increased, medical writers began to
comment on its frequency in different towns and other locations. However, it was only from the
mid-19th century that studies begin to give actual prevalence figures, usually based on patients
seen at the physician’s own hospital.
These clearly show that, by the second half of the 19th century, rickets was a major problem
among the poor in many towns and cities in northern and central Europe. However, using these
sources to investigate social, geographic, or temporal patterns in more detail is fraught with
problems. Although they usually tried to be objective, medical writers could only use the diagnostic
criteria and standards of scientific practice current at the time. This makes it difficult to compare
results of studies written at different times by different authors. This does not mean that they are
not of value in bioarchaeology, but it does mean they must be used with care.
One potential use may be to generate hypotheses that can be tested using bioarchaeological
evidence. For example written sources suggest that, in 19th century England, rickets prevalence
decreased with increasing distance from city centres, and that prevalence was greater in towns with
a strong manufacturing base. With regard to infantile scurvy, they suggest that it may have been
rare in post-mediaeval populations prior to the late 19th century. Bioarchaeology can be used to
investigate the extent to which these patterns can be validated using skeletal data.

resulted in quite a few individuals with pathological conditions being excluded from examina-
tion for the site report. Analysis undertaken as part of a research project demonstrated that
some of the poorly preserved individuals had metabolic bone diseases (Brickley et al., 2007).
Erosion by the physical or chemical actions of soil can remove delicate pathological features,
14 The Bioarchaeology of Metabolic Bone Disease

FIGURE 2–3 Adult female (F284) from the cemetery at Vagnari, Italy. Date of burial CE 150 200. Photo courtesy
of Dr T. Prowse.

and post-depositional breakage allows ingress of soil that can prevent assessment of radio-
graphic features used in assessment of conditions (see Fig. 2 4). Ingress of soil can also
preclude evaluation of bone mineral density using techniques such as DXA (see Chapter 6:
Age-related bone loss and osteoporosis).
Histological investigations can be invaluable for assisting with the diagnosis of pathologi-
cal conditions, but at a microscopic level there may also be changes in archaeological human
bones and teeth that make the study of disease processes difficult. Diagenetic alterations,
such as those shown in Fig. 2 5, can severely disrupt the microscopic appearance of bone.
Diagenetic changes include disruption of mineralised tissue micro-structure by fungi and
bacterial activity, but visual (macroscopic) examination will not allow the detection of such
changes. Bell and Piper (2000) provide an introduction to the use of palaeohistological stud-
ies within bioarchaeology. It is also possible that mineral replacement may take place
(López-Costas et al., 2016), which will render the results of investigations that utilise non-
invasive measures of ‘bone mineral’ inaccurate (Farquharson and Brickley, 1997; Brickley
and Mays, 2019).
Cultural practice regarding treatment of the dead may influence the survival of human
remains. Where societies use designated places to bury individuals, and sites are intensively
used, earlier burials may be disturbed or truncated, as shown in the individuals from an
urban British cemetery shown in Fig. 2 6. In-depth analysis of disease can be hard to under-
take in small mobile band societies. In other groups, funerary processes that involve excarna-
tion and disarticulation, or cremation, have implications for skeletal recovery and evaluation
of lesions. Useful data can be obtained from cremated archaeological bone (e.g. McKinley,
2000), but the amount of information on pathological conditions and biological variables
derived from burned or disarticulated bone will be limited (see images of such material in
Fig. 2 7). To date no cases of metabolic bone disease have been published from cremated
 Chapter 2 • The study of metabolic bone disease in bioarchaeology 15

FIGURE 2–4 Antero-posterior radiograph of part of a femur excavated from an archaeological site. In the lower
part of the picture, large pieces of soil are visible within the medullary cavity, marked by the lower bracket. The
large, transverse post-depositional break, in the middle of the picture, marked by an arrow, shows where soil
entered. The mottled appearance of the radiograph, marked by the upper bracket, shows that soil has infiltrated
the trabecular bone of the metaphysis. Alterations of this sort make it difficult to identify whether any
pathological changes to the trabecular bone were present. In addition, the femur neck is an important area for
bone density measurements for assessing osteoporosis; soil infiltration invalidates such readings, so this bone
would have to be excluded from that type of analysis.
16 The Bioarchaeology of Metabolic Bone Disease

FIGURE 2–5 Backscattered scanning electron microscopy image of diagenetically altered archaeological bone (femoral shaft).
Extensive areas of focal destruction have obliterated most structural features in this piece of archaeological human bone.

bones, and limitations imposed by preservation mean that any cases reported are unlikely to
provide meaningful prevalence data. Although some of the metabolic bone diseases can be
diagnosed from isolated bones that show key lesions used to make a diagnosis, such as pseu-
dofractures in osteomalacia (Brickley and Buckberry, 2015) and the cutting cone in PDB
 Chapter 2 • The study of metabolic bone disease in bioarchaeology 17

FIGURE 2–6 Truncated skeletons from the post-Medieval, St. Martin’ s Churchyard, Birmingham, United Kingdom.
Use of the cemetery was intensive, and, as can be seen in this image, many earlier graves were disturbed by later
burials. Reproduced with permission of CgMs Limited on behalf of the Birmingham Alliance.

(Mays et al., 2017), for the majority of conditions level of skeletal preservation has been
shown to be linked to the likelihood of being able to make a diagnosis in palaeopathology
(Mays et al., 2018). For conditions such as age-related bone loss and osteoporosis, loss of
individuals that experience bone loss in life, combined with problems of accurate identifica-
tion of older individuals, will have a serious effect on reconstructing aspects of health in past
communities.

Techniques for evaluation of archaeological human remains

Macroscopic observation is the foundation for recording of lesions. Use of a hand lens can
assist considerably in picking up post-depositional breakage from features that developed
antemortem, and light and digital microscopy allow higher magnification, with the possibility
of obtaining images that can be used in evaluation.
Plain film radiography can be used to assess aspects of bone loss that have been directly
investigated clinically (Chapter 6: Age-related bone loss and osteoporosis; e.g. Virtama and
Helelä, 1969) and is invaluable in diagnosing cases of PDB (Wittenberg, 2001). The V-shaped
area of radiolucency seen in long bones, often referred to as the cutting cone, is virtually
pathognomonic of PDB (Smith et al., 2002).
18 The Bioarchaeology of Metabolic Bone Disease

FIGURE 2–7 (A) Disarticulated human bone at the third clearance level in the south chamber of Hazleton North, a
Neolithic long Cairn in England. (B) Romano-British lidded urned cremation burial from Dorset, England. Lack of soil
infiltration means the bone has retained the fragment-size as at the time of original deposition. (A) Photograph by
Alan Saville (Saville, A. (Ed.), 1990. Hazelton North, Gloucestershire, 1979 1982. The excavation of a Neolithic long
cairn of the Cotswold-Severn group. London: English Heritage Archaeological Report 13. Historic Buildings and
Monuments Commission for England, p. 82). (B) Courtesy of Jackie McKinley, Wessex Archaeology UK.

Prior to the wide availability of biochemical tests, histology was an important methodol-
ogy employed in clinical diagnosis of many metabolic bone diseases, and until recently
it was considered the gold standard for diagnosing osteomalacia (e.g. Riaz et al., 1992).
Clinically, cells and soft tissue structures provide important information, but in the absence
 Chapter 2 • The study of metabolic bone disease in bioarchaeology 19

of these there is still considerable scope of histological analysis to contribute important infor-
mation on aspects of metabolic bone disease (Ragsdale and Lehmer, 2012; DeBoer et al.,
2013). Examples of uses of this type of analysis are contained in most chapters. Computed
tomography (CT) and micro-CT assessment have been shown to provide some information
previously accessed via thin sections. Colombo et al. (2019) demonstrated micro-CT identifi-
cation of interglobular dentine was possible in archaeological teeth (Chapter 5: Vitamin D
deficiency), and Kesterke and Judd (2019) used micro-CT to demonstrate micro-structural
changes in bone suggestive of PDB (Chapter 8: Paget’s disease of bone).

Palaeodemography and implications for palaeoepidemiology

Consideration of the demographic composition of the available sample is important in order
to fully study the bioarchaeology of the various metabolic bone diseases. Many circum-
stances affect the ‘sample’ that is available for analysis from different cultures; there may be
different burial treatments according to age, sex and/or gender, socio-economic status, or
life-course stage. Such factors should always be considered before drawing any conclusions
from data obtained from archaeological human remains (DeWitte and Stojanowski, 2015;
Milner and Boldsen, 2017; Grauer, 2018).
Frailty caused by diverse conditions, many of which are unknown when dealing with past
groups, will bias the representation of pathological conditions in archaeological human
remains (see Agarwal and Beauchesne, 2011; DeWitte and Stokanwoski, 2015). Extracting
information on the experiences of individuals in past communities from a sample that com-
prises those that died (Milner and Boldsen, 2012a), and starting to consider issues of selec-
tive mortality discussed by Wood et al. (1992) and DeWitte and Stojanowski (2015), require
accurate demographic information. Consideration has to be given to how deceased indivi-
duals with a condition reflect the pattern of community health and levels of disease seen.
This problem is particularly acute in older adults (Milner and Boldsen, 2012b). Osteoporosis
(Chapter 6: Age-related bone loss and osteoporosis) and vitamin D deficiency (Chapter 5:
Vitamin D deficiency) are both observed to be a significant problem of older adults in the
current population where these factors are investigated in economically developed countries.
Difficulties of accurately identifying older adults in past communities make it hard to know
to what extent these patterns are present in archaeological human remains.
Work on techniques that may assist with older adult age estimation in skeletal individuals
is underway. Recent progress has focussed on assessment of dental structures such as
cementum. Acellular extrinsic fibre cementum is deposited in incremental layers on roots of
teeth, is laid down throughout life, and does not remodel (Yamamoto et al., 2016). Each light
and dark pair of alternating bands, observed on a thin section, appears to correspond to a
year of growth and has the potential to provide more accurate estimates of age-at-death than
those currently achievable via analysis of skeletal indicators. As techniques used are opti-
mised, increasingly accurate results are being produced from teeth of living individuals, and
correlation coefficients of over 0.9 have been reported (1 would indicate a perfect relation-
ship) (e.g. Bertrand et al., 2019). The structures that comprise the bands, and the
Another Random Scribd Document
with Unrelated Content
Enoch, 11 Estella, 145 Esther (Van Gilder), 183 Ethel Rae, 79
Everton, 184 Flora (Young), 169 Florence Walton, 76 Genevra, 144
 316 INDEX Corson, Hannah, 78, 295 Corson, Mary Trunk,
184 Corson, Hannah, 88 Corson, Melton G., 79 Corson, Hannah
Elizabeth, 77 Corson, Melvin, 213 Corson, Harriet Emma, 213
Corson, Millicent (Young), 76 Corson, Harris, 228 Corson, Minnie
Alice, 77 Corson, Harvey, 79 Corson, Moriesa Genevra, 144 Corson,
Helen A., 184 Corson, Morris, 144 Corson, Helen Claire, 144 Corson,
Mulford M., 145 Corson, Hobart, 228 Corson, Nora, 77 Corson, Hugh,
146 Corson, Peter, 52 Corson, Ida Stillwell, 145 Corson, Peter. 76
Corson, Isaac Bradway, 76 Corson, Peter Chattin, 76 Corson, Jacob,
52 Corson, Rachel Rebecca, 79 Corson, John, 52 Corson, Rebecca N.
(Chattin), 76 Corson, John Chattin, 79 Corson, Rem, 183 Corson,
John Chattin, 128 Corson, Rhoda M., 137 Corson, John Marvin, 228
Corson, Richard T., 79 Corson, Jonathan, 52 Corson, Robert Risley,
77 Corson, Jonathan, 78, 295 Corson, Rodman, 144 Corson,
Jonathan W., 78 Corson, Ruthanna E. (Finley), 146 Corson, Joseph
Henry, 144 Corson, Sallie May, 145 Corson, Judson Bradway, 77
Corson, Sarah, 77 Corson, Katherine E., 169 Corson, Sarah Elma, 77
Corson, Lake Lucas, 76 Corson, Sarah G., 78 Corson, Learning F., 77
Corson, Sarah H. (Orum), 78 Corson. Lillie Velma, 144 Corson, Sarah
Louisa, 229 Corson, Lizzie (Young), 77 Corson, Sarah (Marshall), 184
Corson, Louisa, 89 Corson, Smith, 137 Corson, Louisa C. (Lake)
Gandy, Corson, Somers, 89 183 Corson, Stella, 89 Corson, Lucas
Bradway, 79 Corson, Sylvester, 144 Corson, Lucas L., 78 Corson,
Sylvester, 228 Corson, Lucius Elmer, 77 Corson, Talitha, 52 Corson,
Luther, 169 Corson, Talitha, 76 Corson, Lydia Ann, 78 Corson,
Thompson S., 79 Corson, Lydia (Lake), 52 Corson, Viola, 76 Corson,
Lydia Lake, 76 Corson, Violet, 184 Corson, Lydia (Lake), 89 Corson,
Violet (Clark), 228 Corson, Mabel, 213 Corson, Walter, 146 Corson,
Mahlon, 228 Corson, William C, 76 Corson, Martha H. Borden, 79
Corson, William Melton, 79 Corson, Martha Henderson (BorCorson,
William Penn, 228 den), 128 Corson, William Wallace, 228 Corson,
Mary, 78 Corson, Youngs, 184 Corson, Mary, 89 Corson, Zora (Sapp),
228 Corson, Mary C. (Chattin), 79 Cosaboom, Marie, 121 Corson,
Mary E., 184 Cotton, Ann (Lake), 34 Corson, Mary Florence, 145
Cotton, Rev. John, 34 Corson, Mary Lenora, 79 Couch, Henry, 89
 INDEX 317 Couch, Maria (Somers), 89 Couenhoven, Wolfert
Gerretse, 244 Couenover, John, 244 Couenover, Sophia, 244
Cowenhoven, Mary, 166 Cowenhoven, Peter, 166 Cowenhoven,
Peter, 244 Cowenhoven, Peter Wolfertse, 244 Craft, Bessie, 213
Craig, Anna Lucille, 194 Craig, Ashley, 194 Craig, Bateman, 194
Craig, Bessie, 194 Craig, Cale C, 194 Craig, Effie (Utter), 194 Craig,
Harriet Emily, 194 Craig, Howard, 194 Craig, Lewis F., 192 Craig,
Lillia, 98 Craig, Nora A. (McGregor), 192 Craig, Oliver, 194 Cranmer,
Clement, 187 Cranmer, Etta P. (Adams), 187 Cranmer, Joel, 187
Crawford, Amanda, 178 Crawford, Catharine, 187 Crawford, Charles,
209 Crawford, Deborah (Nickerson), 209 Crawford, Estelle, 187
Crawford, Florence, 209 Crawford, Frederick, 209 Crawford, Myrtle
(Dennis), 187 Crawford, Patricia, 187 Crawford, Rosella (Lake), 209
Crawford, Victor, 187 Creamer, Florence (Crawford), 209 Creamer,
Frederick L., 209 Creamer, Nelson, 209 Creamer, Ruth, 209 Creavey,
Katharine, 97 Croker, Harriet W., 231 Cronin, Florence May, 214
Cropsey, Phebe Maria, 16 Crowell, Jennie Martin, 121 Crowley,
Samuel E., 170 Crowley, Sarah Talitha (Lee), 170 Cubberly, Eleanor
(Rolph), 22 Cubberly, James, 22 Currie, Alberta (Leeds), 240 Currie,
Fred. P., 240 Currie, Fred. P., Jr., 241 Currie, George F., 240 Currie,
Mathilda Dallas (Haley), 240 Curry, John W., 154 Curry, Leila May
(Steelman), 154 Curtis, Annie H., 83 Curtis, Frances (Brown), 250
Curtis, Rev. John, 169 Curtis, Rachel Elizabeth, 250 Curtis, Rev.
Walter Wells, 250 Dailey, Harry £., 193 Dailey, Hope H. (Alexander),
193 Daily, Sarah D., 233 Dallas, Samuel, 40 Dalles, Mary, 262 Dalles,
Ruth, 262 Danhart, Albert E., 109 Danhart, Chester Irwin, 109
Danhart, Clifford Ross, 109 Danhart, Elizabeth, 109 Danhart, Mary B.
(English) Raymond, 109 Danhart, Thomas, 109 Dare, Altie, 68 Dare,
Arabella (Smith), 67 Dare, David W., 159 Dare, Joseph Henry, 68
Dare, Julia D. (English), 159 Dare, Lizzie, 68 Dare, Rena, 68 Dare,
Richard B., 67 Dare, Somers, 68 Dare, Tillie, 90 Davenport, Minnie,
253 Davis, Belva Lockwood (Smith), 181 Davis, James, 159 Davis,
Julia (Mann), 159 Davis, Rebecca, 159 Davis, Thelma Marie, 181
Davis, Walter, 181
 318 INDEX Davis, William, 45 De Graw, Harold M., 202 De
Graw, Helen (Boice), 202 Deischer, Diana L. (Penston) Rose, 104
Deischer, William, 104 Delancey, Sam, 260 Delavall, Hannah, 10
Dennis, Alice, 110 Dennis, Anna (Wetzel), 91 Dennis, Bertha
(Borton), 91 Dennis, Bertha (Willers), 187 Dennis, Charles, 86
Dennis, Charles E., 91 Dennis, Charles Edwin, M.D., 91 Dennis,
Constant, 69 Dennis, Davis, 90 Dennis, David Duffell, 91 Dennis,
Deborah Etta (Sooy), 86 Dennis, Edna, 187 Dennis, Elizabeth
Garwood, 91 Dennis, Elizabeth (Scull), 86 Dennis, Ellen Fennimore,
90 Dennis, Eva, 86 Dennis, Harry J., 187 Dennis, Hazel, 91 Dennis,
Henry, 86 Dennis, Jane, 69 Dennis, Joel, 90 Dennis, John Walker, 90
Dennis, Laura, 187 Dennis, Margaret, 186 Dennis, Margaret (Risley),
90 Dennis, Mark Wesley, 91 Dennis, Matthew, 90 Dennis, Myrtle, 187
Dennis, Mary Ann, 91 Dennis, Mary Ann (Frambes), 90 Dennis, Mary
(English) Scull-Eaton, 69 Dennis, Olive, 91 Dennis, Rebecca Caroline,
91 Dennis, Ray, 187 Dennis, Sarah Ann (Risley), 90 Dennis, Sarah
Joanna, 91 Dennis, Stella (Simpers), 187 Dennis, Susan Matilda, 187
Dennis, Susan Matilda, 224 De Wolfe, Fred Neland, 198 De Wolfe,
Hattie E. (Stevens), 198 De Wolfe, Winifred A., 198 D'Hillier, May
Jane, 63 Dilks, Ida, 188 Dillahey, Anna, 189 Dillahey, Elizabeth
(Paris), 189 Dillahey, Samuel, 189 Disbrow, Nathaniel, 270 Divins,
Beulah Ann, 111 Dix, Dorothy Virginia, 253 Dix, Elwood Walter, 253
Dix, George, 253 Dix, Jack Frederick, 253 Dix, John A., 253 Dix,
Leola (Adams), 253 Dix, Martha, 253 Dole, Rebecca, 56 Dooley,
Abbie, 148 Doolittle, Jerusha, 143 Doran, Mrs., 25 Doughty, Ann,
284 Doughty, Ann Eliza (Lake), 88 Doughty, Baker, 252 Doughty,
Bertha (Ireland), 252 Doughty, Carrell, 88 Doughty, Clarence, 110
Doughty, Daniel, 88 Doughty, Edna, 110 Doughty, Edward, 110
Doughty, Edward, 206, 284 Doughty, Elmer, 110 Doughty, Esther
(Babcock), 252 Doughty, Flora Bell, 88 Doughty, Fraley F., 252
Doughty, Iva, 110 Doughty, Lewis T., 88 Doughty, Margaret, 206
Doughty, Melvina (Lee), 110 Doughty, Phoebe (Baker), 88 Doughty,
Phoebe Emma, 88 Douglas, Emily Jane, 28 Dowler, Charles Norman,
228 Dowler, Sarah Altina (Clouting), 228 Dragoo, Edith (Miller), 107
Dragstrem, Justa, 45 Drennon, Anna Elizabeth, 248
 INDEX 319 Drennon, Lydia E. (Townsend), 248 Drennon,
Newton, 248 Duberson, Anna Marguerite, 229 Duberson, Elisha C,
229 Duberson, George A., 229 Duberson, Hannah (Price), 229
Duberson, Jay, 229 Duberson, Margaret (Peterson), 229 Duberson,
Mary M., 229 Duerr, Cora, 106 Dunlap, Edith (Tilton), 123 Dunlap,
Tilton, 123 Dunlap, William, 123 Dunn, Amanda (Garsed), 242 Dunn,
Bessie A. (Bullock), 242 Dunn, Garsed Thomas, 242 Dunn, Herbert
or Robert Wilson, 242 Dunn, Herbert Sidney, 242 Dunn, Howard
Garsed, 242 Dunn, Robert or Herbert Wilson, 242 Durfee, Myra, 199
Durfee, Myra (Copeland), 199 Durfee, William, 199 Dutch, Cornelius,
168 Dutch, Emma Jane (English), 168 Dutch, John Albert, 168
Dutch, Rebecca (Price), 168 Dutch, Vera Agatha, 168 Eaton, David,
69 Eaton, Mary (English) Scull, 69 Echman, Eunice E., 170 Echman,
Eunice S. (Lore), 170 Echman, Robert, 170 Eddy, Lucien, 89 Eddy,
Mary (Corson), 89 Edwards, Adolph, 89 Edwards, Daniel, 261
Edwards, Ebenezer, 261 Edwards, Elizabeth (Ingersoll), 135
Edwards, Joseph, 41 Edwards, Joseph, 135 Edwards, Louisa
(Corson), 89 Edwards, Naomi, 135 Edwards, Naomi, 245 Edwards,
Sarah, 124 Edwards, Sarah, 158 Egbert, Mary Ann (Lake), 24 Egbert,
William, 24 Eggman, Elizabeth, 294 Ehmann, Bertha May, 176
Ehmann, Caroline (Suck), 176 Ehmann, Franklin Risley, 176 Ehmann,
Frederick, 176 Ehmann, Frederick Henry, 176 Ehmann, Otto Louis,
176 Ehmann, Sophia Smith (Risley), 176 Filer, Jane, 102 Eisenhart,
Mary E., 147 Eldredge, Charlotte Alice (Young), 141 Eldredge, Harriet
S., 141 Eldredge, Josiah, 141 Eldredge, Marium (Adams), 141
Eldredge, William W., 141 Eldridge, Claude, 101 Eldridge, Elsie May,
101 Eldridge, Harriet T. (Barnes), 101 Eldridge, James, 101 Eldridge,
James Leroy, 101 Eldridge, Margaret McCormick, 101 Eldridge,
Medora (Wilson), 101 Eldridge, Melvin, 101 Eldridge, Samuel S., 101
Elliott, Aaron, 60 Elliott, David, 60 Elliott, David, 94 Elliott, Deborah
Ann (Chambers), 94 Elliott, Ethel May, 94 Elliott, Hannah, 95 Elliott,
Jennie, 95 Elliott, Jesse, 94 Elliott, John, 94 Elliott, Joseph, 60 Elliott,
Joseph, 94 Elliott, Mary, 94 Elliott, Mary, 95 Elliott, Rachel, 94
 320 Elliott, Raymond, 94 English, Asenath, 213 Elliott,
Somers, 95 English, Asenath, 230 Elliott, Sylvia, 94 English, Asenath
C, 162 Elliott, Sylvia (Lake), 60 English, Blanche (Leeds), 168 Elliott,
William, 94 English, Calvin, 169 Ellis, George David, 63 English,
Caroline, 164 Ellis, John D'Hillier, 63 English, Caroline, 167 Emerson,
John, 102 English, Catharine, 168 Emerson, Sarah C. (Utter) Weirs,
English, Charles, 68 102 English, Charles B., 68 Emmons, Elizabeth
(Lake), 15 English, Charlotte (Lee), 107 Emmons, Gertrude Prescott,
99 English, Chauncey P., 161 Emmons, Jacobus, 15 English,
Christopher L., 171 Emmons, James, 98 English, Clark P., 83
Emmons, Jesse, 98 English, Daisy, 161 Emmons, Jesse Ackley, 99
English, Daniel, 67 Emmons, Lillian, 98 English, Daniel, 68 Emmons,
Martin John, 99 English, Daniel L. Steelman, 82 Emmons, Mary, 110
English, Dorcas (Adams), 167 Emmons, Mary Amelia, 99 English,
Dorcas L., 167 Emmons, Mary (Higbee), 99 English, David B., 83
Emmons, Mary J. (Lake), 98 English, David R., 67 Emmons, Mary
(Rutter) Yates, 99 English, Edna, 168 Emmons, Sarah Elizabeth, 98
English, Edwin, 108 Emmons, Virginia Hall, 98 English, Egbert, 83
Endicott, Eliza (Vaughn), 180 English, Egbert, 162 Endicott, William,
180 English, Elijah A., 160 Englehart, Charlotte (Wilson) 108 English,
Elizabeth (Babcock), 68 Englehart, William, 108 English, Elizabeth
(Babcock), 170 Englehart, William F., 108 English, Elizabeth
(Giberson), 68 English, Abel, 109 English, Elizabeth (Gifford), 83
English, Agatha B. (Lake), 168 English, Elizabeth (Mathis), 161
English, Albert, 162 English, Ella, 160 English, Albert. 204 English,
Elmer, 68 English, Albertson L., 162 English, Elnora (Somers), 169
English, Alice J., 159 English, Elvira S. (Conover), 83 English, Alwilda,
168 English, Emeline, 169 English, Andrew R., 171 English, Emeline,
246 English, Ann Elizabeth (English), English, Emeline L., 171 247
English, Emma J., 161 English, Ann W. (Smith), 84 English, Emma J.
(Souders), 162 English, Anna A. (Williams), 161 English, Emma J.
(Souders), 204 English, Anna Mary, 171 English, Emma Jane, 168
English, Anna P. (Champion), 108 English, Esther, 162 English, Anna
Theresa, 162 English, Esther (Collins), 83 English, Annie E., 83
English, Esther Collins, 164 English, Annie H. (Curtis), 83 English,
Esther (Collins), 213 English, Annie S. (Smith), 108 English, Ethel
(Lee), 107 English, Asenath, 167 English, Etta (Asay), 170
 INDEX 321 English, Eunice, 170 English, Julia (Frambes),
160 English, Eva Mae, 169 English, Kate G., 160 English, Ezra, 170
English, Kate G., 236 English, George Earl, 168 English, Kate M.
(Watson), 68 English, George H., 160 English, Katie, 161 English,
George Hilyard, 160 English, Kessie, 245 English, George W., 108
English, Lamer, 83 English, Gertrude, 162 English, Leona, 169
English, Hannah, 68 English, Lettice, 161 English, Hannah (Clift), 53
English, Lettice J., 83 English, Hannah (Clift), 166 English, Lizzie, 68
English, Hannah G., 83 English, Lizzie (Collins), 107 English, Hannah
H., 108 English, Lois, 82 English, Hannah (Holdzkom), 67 English,
Lois L., 161 English, Harriet (Aydelotte), 162 English, Louisa
(Albertson), 162 English, Harriet N., 107 English, Louise, 238
English, Helen, 168 English, Lucy, 161 English, Helen (Madden) ,238
English, Lydia, 68 English, Horace Leeds, 168 English, Lydia, 160
English, Ion, 107 English, Lydia, 170 English, Isaac, 50 English, Lydia
Ann (Scull), 107 English, Isaac, 68 English, Lydia L., 170 English,
Isaac, 169, 170 English, Lydia L., 237 English, Isaac J., 170 English,
Lydia (Lake), 82 English, James, S3 English, Lydia Lake, 160 English,
James, 82 English, Margaret, 68 English, James, 161 English,
Margaret A. (Lake), 82 English, James, 166 English, Margaret C, 160
English, James Edward, 160 English, Margaret van Beek, 68 English,
James Truitt, 167 English, Margaretta, 171 English, Jemima (Lake),
SO English, Marguerite, 162 English, Jemima (Lake), 169 English,
Marietta, 165 English, Jesse, 107 English, Marion, 108 English,
Joanna, 68 English, Mark, 112 English, Johanna, 109 English, Mark,
160 English, John, 53 English, Mark L(ake), 159 English, John, 68
English, Martha B. (Smith), 68 English, John, 83 English, Mary, 68
English, John, 107 English, Mary, 69 English, John, 166 English,
Mary, 107 English, John Peter, 168 English, Mary, 159 English,
Joseph, 53 English, Mary Ann, 162 English, Joseph, 84 English, Mary
A. Quigg, 160 English, Joseph, 166 English, Mary B., 109 English,
Joseph, 171 English, Mary (Barrett), 108 English, Joseph H., 107
English, Mary Connelly, 167 English, Judith, 108 English, Mary E.,
160 English, Judith S. (Robinson), 171 English, Mary Elizabeth, 238
English, Julia D., 159 English, Mary (Ireland), 161
 322 INDEX English, Mary (Lake), 53 English, William, 160
English, Mary (Lake), 166 English, Wilmyra K, 162 English, Mary
(Scull), 67 Erskine, El Freda (Champion), English, Matilda, 160 213
English, Matilda Spear, 165 Erskine, Josephine (Brophy), 213 English,
Mattie (Scull) Steelman, Erskine, Roland Dean, 213 160 Erskine,
Thomas, 213 English, Mayme (Pfeil), 168 Essick, Josephine, 239
English, Melvina E. (Stead), 170 Estell, Martha K., 210 English,
Mildred, 168 Evans, Eliza, 108 English, Minerva B., 68 Ewan, Abbie,
184 English, Miriam (Champion), 107 F English, Mizeal, 167 English,
Morris Cain, 168 Fagan, Emma, 58 English, Morrison, 160
Fairbrothers, Cornelia, 225 English, Nicholas S., 83 Fairbrothers,
David, 225 English, Nora S., 109 Fairbrothers, Earl, 225 English, Ola,
161 Fairbrothers, Edna Freas, 225 English, Paulina, 83 Fairbrothers,
Godfrey, 225 English, Pauline, 162 Fairbrothers, Helen, 225 English,
Peter, 83 Fairbrothers, Katherine, 225 English, Peter, 166
Fairbrothers, Linford, 225 English, Peter, 167 Fairbrothers, Mary B.
(Risley), English, Peter, 213 225 English, Philip, 68 Fairbrothers, Mary
(Freas), 225 English, Prudence, 53 Fairbrothers, Somers L., 225
English, Prudence (Springer), 166 Farnham, Gershom, 125 English,
Ralph, 160 Farnham, Ruby, 125 English, Rebecca (Davis), 159
Farnham, Sarah M. (Albertson), English, Robert A., 159 125 English,
Robert B., 83 Farnham, Walter, 125 English, Rosetta, 158 Feaster,
Elizabeth, 150 English, Rosetta, 210 Feltman, Lorie, 106 EngHsh,
Rosetta S., 159 Fennimore, Ellen, 90 English, Samuel Budd, 237
Fenton, Agnes, 208 English, Sarah, 53 Fenton, Alfred, 208 English,
Sarah, 69 Fenton, Amelia, 208 English, Sarah, 166 Fenton, Anna
Bella, 208 English, Sarah Ann (Smith), 109 Fenton, Anna Bella
(Lake), 208 English, Scull, 68 Fenton, Bertie, 111 English, Scull, 72
Fenton, Edward, 208 English, Somers, 108 Fenton, Edwin, 208
English, Somers, 160 Fenton, Elizabeth, 208 English, Susan, 161
Fenton, Ezra, 208 English, Talitha, 67 Fenton, Ezra A., 208 English,
Talitha, 169 Fenton, George, 208 English, Theodore, 161 Fenton,
Hannah, 208 English, Walter C, 170 Fenton, Hattie, 208 English,
Warren, 108 Fenton, Kenneth, 208
 INDEX 323 Fenton, Linda (Shepard), 208 Fenton, Lorene,
208 Fenton, Lydia Ann (Adams), 111 Fenton, Mabelle, 208 Fenton,
Mamie Metz (Miller), 208 Fenton, Marie, 208 Fenton, Martha, 208
Fenton, Oscar, 208 Fenton, Rachel, 208 Fenton, Rosa, 208 Fenton,
Rose A. (Helferty), 208 Fenton, Samuel, 208 Fenton, Samuel M., Ill
Fenton, Thomas, 208 Fenton, Walter, 208 Ferguson, Arthur Wesley,
215 Ferguson, Carrie L. (Lake), 214 Ferguson, Frances Ruth, 215
Ferguson, Grace Lorena, 215 Ferguson, Helen Mildred, 215
Ferguson, James Ralph, 215 Ferguson, Marian Luella, 215 Ferguson,
Norman Everett, 215 Ferguson, Rev. William Alexander, 214
Ferguson, William Byron, 215 Fessler, Effie E. (Tilton), 192 Fessler,
George M., 192 Fifield, Abigail, 211 Fifield, Abigail (Tilton), 122
Fifield, Clara, 211 Fifield, Clara (Smith), 211 Fifield, Elva F., 211
Fifield, Emma, 211 Fifield, Capt. John C, 122 Fifield, Capt. John C,
123 Fifield, Lillie Belle (Bartlett), 211 Fifield, Mary G. (Somers), 211
Fifield, Sarah Jane (Tilton), 122 Fifield, Sarah Jane (Tilton) Imlay,
123 Fifield, Walter, 211 Fifield, Walter J., 211 Finch, diaries, 62 Finch,
Eva, 62 Finch, Hester, 62 Finch, Judith (Hess), 62 Finch, Lorena, 62
Finch, Ralph, 62 Finch, Walter, 62 Finch, William, 62 Finley,
Ruthanna E., 146 Fish, Alexander, 163 Fish, Alexander, 259 Fish,
Elizabeth Ann, 136 Fisher, Edward, 68 Fisher, Ellen J. (Leeds) Baker,
196 Fisher, Isaac E., 68 Fisher, John, 196 Fisher, Lydia (English), 68
Fisher, Mary Margaret, 180 Fisher, Sarah, 93 Reming, Abigail, 84
Fleming, Ann C. (Collins), 84 Fleming, Rev. Caleb K., 84 Fleming,
Emma H. (Stanger), 85 Fleming, John, 84 Fletcher, How^ard Egbert,
227 Fletcher, James W., 227 Fletcher, James Wilson, 227 Fletcher,
Miranda D. (Lake), 227 Fletcher, Robert Vincent, 227 Fletcher, Ruth
Eva, 227 Foltz, Charles Tage, 152 Foltz, Ethel Mae (Tage), 152 Foltz,
Thomas Franklin, 152 Ford, Eleanor, 144 Fortiner, Florence Shivers,
248 Foster, Charles, 88 Foster, Clara (Ludlam), 88 Foster,
Constantine, 88 Foster, Edward, 78 Foster, Ellen, 88 Foster, Mary
(Lake), 88 Foster, Nicholas, 88 Foster, Pauline (Stites), 88 Foster,
Sarah, 88 Fowler, Edwin, 61 Frambes, Ann, 87 Frambes, Eliza
(Price), 160 Frambes, Elizabeth, 210 Frambes, Ellen (Wright), 142
Frambes, Emily, 200 Frambes, Elva Leroy, 122 Frambes, Eva W., 142
Frambes, Ezra A., 210 Frambes, Ezra D., 210 Frambes, Fransanna,
80
 324 INDEX Frambes, Hannah R, 122 Frambes, Hannah
(Ireland), 80 Frambes, Hannah (Irelan), 122 Frambes, Harriet Jane,
210 Frambes, Japhet I., 160 Frambes, Job, 80 Frambes, Job, 122
Frambes, John, 56 Frambes, Lillian (Fierson), 210 Frambes, Margaret
Tilton, 210 Frambes, Mary Ann, 90 Frambes, Mary (Tilton), 122
Frambes, Peter Tilton, 142 Frambes, Richard I., 122 Frambes, Sarah
E. (Adams), 210 Frambes, Susan D., 182 Freas, David, 225 Freas,
Mary, 225 French, Adelaide L. (Pinyard), 248 French, Alice Matilda,
172 French, Alma Ashley (Cavileer), 172 French, Bessie Virginia, 172
French, Caroline Elizabeth, 249 French, Courtland T., 172 French,
Emma Belle, 172 French, Florence Howard, 249 French, Genevieve
Adelaide, 249 French, Hannah E. (Corson), 11 French, lona, 172
French, Ivy (Thamberlin, 11 French, Mary Caroline (Collins), 172
French, Peter Chattin, 11 French, Phoebe (Mathis), 172 French,
Samuel J. Tilden, 172 French, Smiley, 11 French, Theodore Tilden,
249 French, Thomas S., 11 French, William, 172 French, William
Collins, 248 French, William Collins, 249 French, William Nelson, 172
French, Woodrow Wilson, 249 Fuhrer, Mary, 176 Furman, Eleanor, 32
Furman, Rosalie Allen, 248 Fry, Mary A., 142 Fry, Mary A., 251
Gabbeart, Lucinda (Parr), 193 Gabbeart, Lydia E. (Tilton) Chapman,
193 Gabbeart, Miles L., 193 Gabbeart, William, 193 Gale, Dinah, 206
Gale, Mary, 206 Gale, Samuel, 206 Galkler, Columbia, 98 Gallagher,
Anna Ridgeway, 173 Gallagher, Harriet (Begg), 173 Gallagher, John,
173 Gallaher, Emily B. (Eldridge), 101 Gallaher, Frank S., 101
Gallaher, Ralph E., 101 Gallup, Hannah (Lake), ZZ Gallup, John, ZZ
Gandy, Almeda, 183 Gandy, Elizabeth (Strickland) Weed, 183 Gandy,
Ellen (Foster), 88 Gandy, Hannah, 86 Gandy, John G., 183 Gandy,
John G., Jr., 183, 295 Gandy, Laura (Bennett), 183 Gandy, Louisa C.
(Lake), 183 Gandy, Lydia (Gillingham), 183 Gandy, Oliver M., 183
Gardiner, George King, 226 Gardiner, Louise (Jockel), 226 Gardiner,
Mary Bell (Lake), 226 Gardiner, William F., 226 Gardiner, William
John, 226 Garnick, Alwilda (English) Smith, 168 Garnick, Julius, 168
Garrard, Ella Este, 79 Garrard, Harrold L. Crater, 79 Garrard, James
H., 79 Garrard, Rachel Rebecca (Corson), 79 Garrard, Sarah, 79
Garrard, William T., 79 Garretson, Harmanis, 20 Garretson, Mary, 78
Garretson, Phebe, 144, 145 Garrison, Ada, 170
 INDEX 325 Garrison, Ann, 22 Garrison, Caroline L., 59
Garrison, Caroline (Lake), 59 Garrison, Charles, 170 Garrison, Elva,
59 Garrison, Dr. H. C, 64 Garrison, James, 59 Garrison, Jane Dennis,
69 Garrison, Lina (Bailey), 59 Garrison, Lucy (Tullis), 64 Garrison,
Lydia L. (English), 170 Garrison, Margaret H., 59 Garrison, Mary L.,
59 Garrison, Mary L., 263 Garrison, Mary Lee, 59 Garrison, Melvina
L, 170 Garrison, Norton, 59 Garrison, Phoebe (Parsons), 59 Garrison,
Rachel, 45 Garrison, Robert, 59 Garrison, Robfert L., 59 Garrison,
Ruth W., 59 Garrison, William, 69 Garrison, William Lummis, 59
Garsed, Amanda, 242 Garton, Charles Franklin, 252 Garton, Harry,
252 Garton, Harry Franklin, 252 Garton, Belle (Hackett), 252 Garton,
Myrtle S. (Blackman), 252 Garton, Peter, 121 Garton, Russell Lewis,
121 Garton, Samuel, 121 Garton, Susanna (Lake), 121 Garwood,
Almira, 174 Garwood, Almira (Babcock), 87 Garwood, Almira
(Babcock), 197 Garwood, Aura, 197 Garwood, Elizabeth, 56
Garwood, Emma, 168 Garwood, Joshua, 56 Garwood, Lois (English),
82 Garwood, Margaret, 52 Garwood, Margaret, 166 Garwood,
Margaret Collins, 87 Garwood, Mary, 52 Garwood, Mary, 148
Garwood, Mary (Ballinger), 166 Garwood, Rebecca (Dole), 56
Garwood, Richard, 87 Garwood, Richard, 174 Garwood, Richard, 197
Garwood, Sarah, 82 Garwood, Thomas, 51 Garwood, Thomas, 82
Garwood, Thomas, 166 Gaskill, Deborah, 52 Gaskill, Edward, 109
Gaskill, Elizabeth (Robinson), 109 Gaskill, Elsa, 109 Gaskill, Horace,
109 Gaskill, Judith (Somers), 109 Gaskill, Lillian, 109 Gaskill, Mary
Holland, 127 Gaskill, Melvin, 109 Gaskill, Robert, 109 Gaunt, Amelia
(Fenton), 208 Gaunt, Bessie, 208 Gaunt, Catherine, 208 Gaunt,
David, 208 Getz, Louisa, 227 Gibb, Anna, 225 Gibbs, Byron, 105
Gibbs, Edwin, 105 Gibbs, Hannah, 105 Gibbs, Justice, 105 Gibbs,
Lawrence, 105 Gibbs, Lydia J. (Laman), 105 Gibbs, Mary, 105 Gibbs,
Sarah (Penston), 105 Giberson, Elizabeth, 68 Giberson, Esther, 174
Giberson, Mary, 84 Gifford, Elizabeth, 83 Giflford, Hannah, 165
Gilbert, Albert Cecil, 231 Gilbert, Albert G., 231 Gilbert, Florence May
(Lake), 231 Gilbert, Irena, 231 Gilbert, Morella, 127 Gilbert, William
Lake, 231 Gilkerson, Bertha, 193 Gilkey, Eleanor M., 210 Gilkey,
James A., 210 Gilkey, Marguerite, 210 Gilkey, Mary, 210 Gillingham,
Edwin, 183 Gillingham, Hannah, 66
 326 INDEX Gillingham, Lydia, 183 Gillingham, Sarah
(Merrill), 183 Gillingham, Yeamans, 66 Gilmore, Mary, 214 Gilsey,
Mary (Stiles), 230 Gilsey, Rena, 230 Gilsey, Samuel, 230 Ginther,
Clyde, 106 Ginther, Lizzie, 107 Ginther, May (Mason), 106 Glan,
Gabriel, 264 Glasby, Rachel, 47 Gleen, Gabriel, 262 Glick, Barbara
(Mast), 186 Glick, Benjamin F., 186 Glick, Elias Walton, 186 Glick,
Frances Barbara, 186 Glick, Halvor Harley, 186 Glick, Jonathan, 186
Glick, Maudena (Mason), 186 Glick, Raymond Augustus, 186 Glick,
Robert Laird, 186 Gobel, Anna May, 246 Godbou, Anna Pauline, 249
Goddard, Betsy Ann Floretta, 11 Godfrey, Betsy (Miller), 144 Godfrey,
Charlotte W. (Corson), 229 Godfrey, Comfort (Phillips), 229 Godfrey,
Ellen, 144 Godfrey, Esther, 89 Godfrey, Hannah (Gandy), 86 Godfrey,
Hiram, 86 Godfrey, Irene C, 229 (jrodfrey. Learning, 229 Godfrey,
Mulford T., 229 Godfrey, Olive (Lake), 89 Godfrey, Townsend, 144
Godfrey, Townsend, 229 Godfrey, William, 89 Godfrey, William P., 229
Godfrey, Velma, 229 Golden, Anna (Brown), 174 Golden, Catherine,
174 Golden, Thomas, 174 Golden, William, 36 Golding, Martha, 212
Good, Jessie, 78 Good, Lewis, 98 Good, Virginia H. (Emmons), 98
Goodbartlett, Agnes (Mungal),166 Goodbartlett, Elizabeth, 166
Goodbartlett, Oswald, 166 Goodyear, Mary, 34 Gooth, Margaret, 207
Gordanier, Amy, 27 Gordon, Amy Ellen, 105 Gordon, Mary Louisa
(Utter), 105 Gordon, Robert Abraham, 105 Gordon, Robert Squire,
105 Gordon, Walter Spafford, 105 Gorham, Ella Este, 78 Gorham,
Hannah G., 78 Gorham, Sarah G. (Corson), 78 Gorham, Sarah Lizzie,
78 Gorham, Timothy, 78 Goulding, Hester, 31 Goulding, John, 31
Goulding, Margaret (Lake), 31 Goulding, Mary, 31 Goulding, Samuel,
31 Goulding, Sarah, 31 Goulding, William, 8 Goulding, William, 31
Grandvaux, Edna, 162 Grandvaux, Louis J., 162 Grandvaux, Wilmyra
E. (English), 162 Gray, Albert, 69 Gray, Elizabeth Babcock, 69
Greaves, Martha, 259 Green, Adaline Springer, 173 Green, Maria Ann
(Saylor), 173 Green, Martin Lodge, 173 Green, Mary, 255 Green,
Sophia, 45 Greenhill, Rebecca, 165 Greenhill, Samuel, 165
Greenwood, Bertha (Utter), 191 Greenwood, George, 191
Greenwood, Mabel, 191 Greenwood, Richard, 191 Greinert, Anna
Augusta, 158 Grey, Mary, 177 Griffiths, Sarah, 54 Grigg, Edward S.,
237 Grigg, Helen S., 237 Grigg, Herbert, 237
 INDEX 327 Grigg, Kate G. (English), 237 Grigg, Lincoln, 237
Grigg, Ralph E., 237 Griscom, Isaac N., M.D., 247 Griscom, Lillian B.
(Scull), 247 Griscom, Marie R., 247 Guden, Florence C., 17 Guyon,
James, 22 Gwin, Sarah, 111, 168 H Haas, Emma Josephine
(Ledterman), 157 Haas, Herbert Eugene, 157 Haas, John Smith, 157
Haas, LilHan (Scheldine), 157 Haas, Louise Hannah (Bumstead), 157
Hackett, Alberta (Lake), 226 Hackett, Belle, 252 Hackett, Constant,
226 Hackett, Eliza, 174 Hackett, Elizabeth (Hildreth), 226 Hackett,
George L., 239 Hackett, Harry W., 226 Hackett, Irma Marie, 226
Hackett, John, 239 Hackett, Josephine, 227 Hackett, Lucinda, 161
Hackett, Martha, 239 Hackett, Nellie M. (Ingersoll), 239 Hackett,
Phebe Emily (Price), 235 Hackett, Ralph, 235 Hackney, Rejoice, 175
Hadden, Ruth, 103 Haigh, Brooks, 176 Haigh, Catharine (Mathis),
176 Haigh, Hazel, 176 Hale, Byron Rogers, 238 Hale, Harriet Lois
(Rogers), 238 Hale, Senator, 220 Hale, Taylor Kyle, 238 Haley,
Caroline, 57 Haley, Mathilda Dallas, 240 Hall, Grace Sullivan, 155
Hall, Henry, 43 Hall, Henry, 263 Hall. Lois S., 238 Hall, Mary, 43 Hall,
Mary, 263 Hall, William, 43 Hall, William, 263 Hallam, Daniel, 91
Hallam, Florence (Cooper), 91 Hallam, Thomas G., 91 Hallbright,
Rose, 182 Hand, Caroline, 59 Hand, Daniel, 59 Hand, Elias, 44 Hand,
Ida B., 59 Hand, Mary (Lake), 44 Hand, Ruth W. (Garrison), 59
Hand, Silvea, 262 Hand, WiUiam N., 59 Hanthorne, Bathsheba, 65
Hanthorne, Isaac, 65 Hanthorne, John, 65 Hanthorne, Mary D., 101
Hanthorne, Mary (Lake), 65 Hanthorne, Robert H., 65 Hanthorne,
Simon, 65 Harbin, Hugh Francis, 194 Harbin, Marie (Utter), 194
Harbin, Mary Frances, 194 Harford, Dorothy, 199 Harkins, Catharine
(Lake), 294 Harkins, John, 294 Harmer, Frank, 234 Harmer, Lulu
(Lewis), 234 Harris, Capt., 290 Harris, Elizabeth Lake (Nuneviller),
100 Harris, Herbert Manson, 100 Harris, Lillian Laura, 100 Harris,
Martha (Lake), 33 Harris, Mary Ellis, 100 Harris, Phoebe Belle, 140
Harris, Thomas, 33 Harris, Walter, 100 Hart, Clara S. (Sooy), 182
Hart, Harry, 182 Hartshorne, Anna, 108 Harvey, Adelaide H., 79
Harvey, James H., 79 Hassell, Mariah, 193 Hatton, Erva Wallette, 226
Hatton, Irma M. (Hackett), 226
 328 INDEX Hatton, Walter B., 226 Hauenstcin, Elizabeth,
246 Hauenstein, Ella, 246 Hauenstcin, Kaster, 245 Hauenstein,
Kessie (English), 245 Hauenstein, Mary, 246 Hauenstein, Mary Ann,
245 Hauenstein, William, 245 Hawkins, May Pauline, 230 Hayes,
Mary Emma, 183 Hayward, Mary Ann, 195 Haywood, Anna May
(Gobel), 246 Haywood, Annie L. (Scull), 246 Haywood, Clarence, 246
Haywood, Gardiner, 246 Haywood, Harold, 246 Haywood, Milton,
246 Headley, Effie C. (Adams), 225 Headley, Gertrude L. (Price), 230
Headley, (Anthony) Harry, 230 Headley, Helena Belle, 230 Headley,
Helena (Pharo), 230 Headley, Kathryn Electa, 225 Headley, Laban,
225 Headley, Louis Milton, 225 Headley, Raymond Everett, 225
Headley, Samuel C, 230 Headley, Vera Ellen, 225 Heath, Lewis, 13
Heaton, Abigail, 40 Helferty, Rose A., 208 Henderson, Mary E., 208
Hentz, Eva, 190 Henneberger, Qara Virginia, 190 Henneberger,
Elmina V. (Utter), 190 Henneberger, Francis J., 190 Henneberger,
Lawrence F., 190 Henneberger, Lawrence Robert, 190 Hepner, David,
209 Hepner, Esther Coney, 209 Hepner, Ezraetta (Lake), 209 Hepner,
Frank L., 209 Hepner, George F., 209 Hepner, Jacob L., 209 Hepner,
Joseph K., 209 Hepner, Martha E., 209 Hepner, Roland F., 209
Hepner, Walter L., 209 Hepner, William F., 209 Hess, Aaron, 62 Hess,
Edward, 62 Hess, Elizabeth, 63 Hess, Ellen, 60 Hess, Frederick, 60
Hess, Garner T., 63 Hess, Hannah (Lake), 62 Hess, Horace B., 62
Hess, Jesse, 63 Hess, Judith, 62 Hess, Martha, 62 Hess, Mary, 62
Hess, Mary Scull, 60 Hess, Sophia Lake, 99 Hess, William, 63
Hickman, David, 69 Hickman, Enoch, 69 Hickman, Esther, 69
Hickman, Eva (Dennis), 86 Hickman, Harriet (Brown), 69 Hickman,
Henry, 69 Hickman, Jemima, 69 Hickman, Joseph, 86 Hickman,
Lorenzo, 69 Hickman, Margaret, 69 Hickman, Mariam, 69 Hickman,
Martha, 69 Hickman, Mary, 69 Hickman, Mary, 110 Hickman, Sarah,
69 Hickman, Sarah (English), 69 Hickman, Thomas H., 69 Hickok,
Beatrice Adelaide, 167 Hickok, Dorcas L. (English), 167 Hickok, Eliza
(Barney), 167 Hickok, Melvin D., 167 Hickok, Reuben, 167 Hicks,
Sarah, 23 Higbee, Fannie, 54 Higbee, James Edward, 105 Higbee,
Jennie (Scull), 97 Higbee, Mary, 99 Higbee, Mary (Gibbs), 105
Higbee, Silas, 99 Higbee, William S., M.D., 97 Hildreth, Elizabeth, 226
Hinchliffe, Sarah A., 101 Hines, Clara, 131
 INDEX 329 Hines, Susan, 58 Hinkle, C. Alice (Barrett), 253
Hinkle, S. Cameron, 253 Hirst, Ambrose, Id Hirst, Beatrice, Id Hirst,
Beulah D. (Corson), 76 Hirst, Eleanor, 76 Hobbs, Sylvia, 156
Hodgkins, Hannah, 244 Hoffman, Ella Walton, 76 Hoffman, Rebecca,
146 Hogate, Eva (Cain), 61 Hogate, Florence, 61 Hogate, Lizzie, 61
Holden, Earl Russel, 212 Holden, Jannit, 212 Holden, Kathryn, 212
Holden, Maud Virginia (Reed), 212 Holdzkom, Christian, 67
Holdzkom, Susannah (Steelman), 67 Hollenbeck, Sarah E., 227
HoUoway, Henry Harrison, 64 Holloway, Matilda May (Tullis),64
Holloway, Rev. Thomas Pawling, 64 Holmes, Fred S., 126 Holmes,
Pauline, 126 Holmes, Samuel, 18 Homan, Andrew, 42 Homan, Lizzie,
110 Homan, Samuel, 284 Homan, Sophia, 252 Hommer, Augusta E.
(Leeds), 196 Hommer, Barbara, 197 Hommer, Charles Edwin, 196
Hommer, Charles Leeds, 197 Hommer, Flora Myrtle, 197 Hommer,
Lucille E. (Stringer), 197 Hommer, Sara Abigail, 197 Hoopey, Frank,
69 Hoopey, Lizzie E. (Scull), 69 Horton, Charles Mahlon, 60 Horton,
Edward, 60 Horton, Phebe (Stebbins), 60 Housenick, Blanche E., 100
Housenick, Qara (Yost), 100 Housenick, Theodore, 100 Houser,
Dorothy, 168 Houser, Edna (English), 168 Houser, George, 168
Houser, Leroy, 168 Howels, Ruth, 251 Howlett, Ethel, 153 Howlett,
Harry, 153 Howlett, Maud L. (Adams) Miller, 153 Howlett, Robert,
153 Hoxey, Mercy, 115 Hubbard, Arreantie, 13 Hubbard, Bernardus,
11 Hubbard, Elias, 11 Hubbard, Margaret (Lake), 11 Hubbard, Neltie
(Lake), 11 Hubbs, Edward, 64 Hubbs, Lizzie (Pashley), 64 Hubbs,
Walter, 64 Huber, Gertrude (Albertson), 179 Huber, Levi Albertson,
179 Huber, Samuel F, 179 Hudson, Ann, 188 Hulce, Alice Lavina
(Parkyn), 155 Hulce, Alice Mary, 155 Hulce, Beatrice Louise, 156
Hulce, Charles Parkyn, 155 Hulce, Gara B. (Macintosh), 156 Hulce,
Dorothy Grace, 156 Hulce, Elisha, 155 Hulce, George William, 156
Hulce, Grace Sullivan (Hall), 155 Hulce, Jennie Alice, 155 Hulce,
Leola Belle, 156 Hulce, Marion Elizabeth, 155 Hulce, Viola
(Robinette), 156 Hull, Jane, 12 Hull, Winifred (Lake), 12 Humphries,
May, 86 Hunt, Lulu, 188 Huntley, Alice C, 199 Huntley, Capt. John,
199 Huntley, Mary (McCollum), 199 Hurlbut, Levi, 282, 283
Hutchinson, Jane, 63 Huyk, Elizabeth, 13 Huyk, Peter, 13
 330 INDEX Imlay, Abigail (Adams), 123 Imlay, Caroline T.,
124 Imlay, Gideon T., 123 Imlay, Horace Gideon, 124 Imlay, Irene
(Tilton), 124 Imlay, John F., 124 Imlay, Lewis Tilton, 123 Imlay,
Reading, 123 Imlay, Sarah Jane (Tilton), 123 Ingersoll, Ann
(Morgan), 147 Ingersoll, Anna Eliza, 147, 203 Ingersoll, Benjamin,
89 Ingersoll, Daniel, 41, 70, 147 Ingersoll, Denman Bevis, 101
Ingersoll, Dorcas (Smith), 238 Ingersoll, Ebenezer, 41 Ingersoll,
Elizabeth, 135 Ingersoll, Elizabeth, 294 Ingersoll, Emma L. (Skirm),
190 Ingersoll, Eva Hentz, 190 Ingersoll, Hannah, 135, 245 Ingersoll,
Harriet Williams (Risky), 238 Ingersoll, John B., 238 Ingersoll,
Joseph, 42, 86, 101, 295 Ingersoll, Isaac, 85, 164 Ingersoll, Martha
(Lake), 89 Ingersoll, Mary, 42 Ingersoll, Mary Ann, 85 Ingersoll,
Mary D. (Hanthorne), 101 Ingersoll, Millicent (Steelman), 85, 164
Ingersoll, Nellie May, 239 Ingersoll, Norris A., 238 Ingersoll, Rachel
Bevis, 86, 101 Ingersoll, Robert H., 189 Ingersoll, Susannah, 41
Ingersoll, Tabitha, 238 Ingersoll, Tabitha W., 86 Inman, Nellie, 126
Inman, Sarah, 125 Ireland, Alice, 112 Ireland, Anthony, 284 Ireland,
Bertha, 252 Ireland, Bessie, 253 reland, Charles, 62 reland,
Christiana (Lake), 294 reland. Comfort, 206 reland, Deborah, 87
reland, Dorcas, 55, 69 reland, Edmond, 294 reland, Edmund, 55, 90
reland, Ella (Brown), 253 reland, Evalena. 250 reland, Frances, 207
reland, Frank, 62 reland, Hannah, 122 reland, Hannah, 80, 253
reland, Hannah (Lake), 294 reland, Israel, 161 reland, James, 294
reland, John, 250 reland, Joseph, 252 reland, Keturah, 7Z reland,
Lizzie, 62 reland, Lucinda (Hackett), 161 reland, Margaret (Bowen),
252 reland, Mary, 161, 210 reland, Mary Jane (Lake), 62 reland,
Mary (Sampson), 250 reland, Minnie (Davenport), 253 reland.
Nelson, 62 reland, Raymond G., 253 reland, Richard S., 62 reland,
Russell, 253 reland, Ruth, 141 reland, Samuel, 252 reland, Samuel
Warren, 253 reland, Sarah, 259 reland, Sarah Ann, 155 reland, Sarah
Ann (Lake), 90 reland, Sarah (Lake), 39 reland, Sophia (Homan),
252 reland, Tabitha (Lake), 294 reland, Thomas, 90 reland,
Townsend, 90 reland, Walter, 253 reland, William, 62 rish, Rebecca,
27 rvin, Ellen M., 119 rvin, Martha (Alexander), 120 rvin, Thompson,
119, 120 szard, Reeves, 250
 INDEX 331 Jackaway, Hosea Casto, 245 Jackaway, Mary
Jane, 243, 245 Jackaway, Sarah (Surran), 245 Jackson, Charles, 200
Jackson, Charles Edward, 232 Jackson, Lettie, 203 Jackson, Mary E.
(Blake), 200 Jackson, Polly W. Stevens, 232 Jackson, Emma
Elizabeth, 200 Jackson, Gertrude E., 232 James, Bertha, 106 James,
C. H., 106 James, Clara, 106 James, Constant, 90 James, Ella, 106
James, Maria (Mundy), 106 James, May (Laird), 90 James, Thomas,
106 Janse, Court, 31 Janse, Hendrick, 31 Janse, Elizabeth (Lake), 31
Janse, Maria, 31 Janse, Phebe, 31 Jeflfers, Andrew B., 180 Jeffers,
George B., 181 Jeffers, Martha L. (Barrett), 180 Jeffers, Susan, 180
Jeffers, Susan B. (Scull), 180, 181 Jeffers, William, 180, 181 Jeffers,
William Lindley, 180 Jeffries, Abigail B., 178 Jeffries, Anna (Dillahey)
189 Jeffries, Annie, 142 Jeffries, Caroline (Lewis), 251 Jeffries,
Christiana, 150 Jeffries, Claude D., 189 Jeffries, Daniel J., 95 Jeffries,
Edmund, 56 Jeffries, Ella, 188 Jeffries, George, 251 Jeffries, Hannah,
150 Jeffries, Harriet L (Smith), 56 Jeffries, John, 150 Jeffries, Laura,
251 Jeffries, Luther, 189 Jeffries, Norman, 189 Jeffries, Rae, 189
Jeffries, Rebecca (Risley), 95 Jeffries, Robert L., 188 Jeffries, Sarah,
56 Jeffries, Sophia (Lake), 95 Jeffries, William, 95 Jenkins, Byron, 81
Jenkins, Mary H. (Parkyn), 81 Jenkins, Rev. Nathaniel, Z7 Jerrell,
Adaline, 57 Jester, Emily J., 251 Jester, Sarah Elizabeth, 251 Jester,
William, 251 Jockel, Louise, 226 Johns, Carrie R. (Shemelia), 152
Johns, David, 153 Johns, George, 152 Johns, Gertrude Rose, 153
Johns, Hattie May, 152 Johns, Phebe Lenora (Lake), 152 Johns,
William Ward, 152 Johnson, Almira C. (Lake), 88 Johnson, Alphie,
112 Johnson, Annie M., 79 Johnson, Asbury, 79 Johnson, Bessie
Virginia (French), 172 Johnson, Cassandra, 79 Johnson, Charles, 213
Johnson, Dewey, 88 Johnson, E. Clinton, 172 Johnson, Eleanor
(Lake), 13 Johnson, Elizabeth (Lake), 14 Johnson, Elsie (Conover),
177 Johnson, Harriet S. (Bryant), 7Z Johnson, Hendrick, 14 Johnson,
Henrietta, 129 Johnson, John, 202 Johnson, Kate (Webb), 213
Johnson, Marie (Utter) Harbin, 194 Johnson, Mildred, 202 Johnson,
Morton, 202 Johnson, Nelson E., 202 Johnson, Nettie (Bryant), 213
Johnson, Nicholas, 15 Johnson, Oscar, 177 Johnson, Ralph Bryant,
213 Johnson, Sarah (Adams), 202 Johnson, Sarah E. (Bartlett), 202
 332 INDEX Johnson, Sarah (Lake), 11 Johnson, Solomon,
IZ Johnson, Walter Roy, 194 Johnson, William N., 202 Johnson,
Yorneche (Lake), 15 Jones, Alice Alethia, 237 Jones, Charles, 181
Jones, Charles William, 237 Jones, Edgar Francis, 237 Jones, Estella
(Smith) Mounce, 181 Jones, Harland C, 102 Jones, Henry, 181
Jones, Kittie Lee, 237 Jones, Lydia Scull, 237 Jones, Margaret Ann
(Scull), 237 Jones, Margaret (Tilton), 102 Jones, Mary R, 111 Jones,
Matilda, 181 Jones, Sallie Ann, 237 Jones, Sydney Everett, 237
Jones, Virginia Lettice, 237 Jones, William E., 237 Joslin, Anna M., 59
Joslin, Catherine, 186 Justice, S., 284 Karsch, Camilla (Utter), 194
Karsch, George D., 194 Karsh, Marie, 175 Kassan, Frances A. (Utter),
103 Kassan, Frank, 103 Kates, Maggie, 62 Kearney, Jennie, 148
Kears, Eliza, 99 Keeler, Harry, 251 Keeler, Mary (Smith), 251 Keeler,
Myrtle, 251 Kellem, Artamissa, 240 Kelly, Adelaide, 154 Kelly,
Adelaide S. (Lake), 154 Kelly, Armenia (Bartlett), 203 Kelly, Charles
LeRoy, 151 Kelly, Erasmus, 97 Kelly, Frank, 203 Kelly, George, 154
Kelly, Harriet E. (Beaman), 105 Kelly, Howard, 154 Kelly, Jennie S.
(Lewis), 151 Kelly, Leicester Leroy, 105 Kelly, Mary, 154 Kelly,
Raymond, 105 Kelly, Sarah (Sprague), 151 Kelly, Thomas, 154 Kelly,
Thomas H., 154 Kelly, William, 151 Kerbaugh, C Roland, 101
Kerbaugh, Charles F., 101 Kerbaugh, Edith Marshall (Lake), 101
Kerbaugh, Sarah A. (Hinchliffe), 101 Kersey, Flora M. (Hommer), 197
Kersey, Myrtle Evelyn, 197 Kersey, Vierling, 197 Key, Augustus, 186
Key, Carrie L. (Mason), 186 Key, Lulu Mason, 186 Kieflfer, Mary E.
(Tilton), 104 Kindle, Daniel, 294 Kindle, Mary Ann (Lake), 294 King,
Amanda E., 142 King, Arabella, 251 King, Charles L., 142 King,
Charles L., 251 King, Mary A. (Fry), 142 King, Mary A. (Fry), 251
Kingsland, Alida (Mesereau), 21 Kingsland, Daniel, 21 Kingsland,
Lydia Alice (Lake), 143 Kingsland, Nathan, 143 Kirk, Edna M., 203
Kirk, Julia (Bartlett), 202 Kirk, Mabel, 203 Kirk, Winfield Scott, 202
Kirk, Winfield Scott, 203 Kite, Minnie, 114 Kniffin, Sarah Jane Totton,
240 Knight, Mae, 210 Knott, Alwilda (Lake), 88 Knott, Idella, 88
Knott, John, 88 Knott, Pauline, 88 Koegley, Emma L., 106
Kronenwetter, Catherine, 228
 333 Kuster, E. B., 104 Kuster, Sarah E. (Tilton), 104 Lacer,
Alice, 107 Lacer, Alice (Miller), 107 Lacer, William, 107 Laird, Abbie
M. (Connelley), 90 Laird, Alfred, 89 Laird, Annie, 90 Laird, Carl, 90
Laird, Catharine (Lake), 89 Laird, Dorothy, 89 Laird, Enoch, 89 Laird,
Frances, 90, 186 Laird, Hannah (Couch), 90 Laird, Harriet, 185 Laird,
Jane (Murphy), 89 Laird, John, 90 Laird, May, 89 Laird, Reuben, 89
Laird, Robert B., 90 Laird, Samuel, 89 Laird, Tillie Dare, 90 Lake,
Abbie, 232 Lake, Abbie Dooley, 148 Lake, Abbie Price (Burroughs),
150 Lake, Abel Adams, 152 Lake, Abigail, 50 Lake, Abigail (Adams),
51 Lake, Abigail (Adams), 87 Lake, Abbie (Adams), 275 Lake, Abigail
(Garrison) Robbins, 59 Lake, Abigail (Heaton), 40 Lake, Abigail
(Robbins), 94 Lake, Abraham, 11 Lake, Abraham, 13 Lake, Abraham,
17 Lake, Abraham, 19 Lake, Abraham, 20 Lake, Abraham, 21 Lake,
Abraham, 40 Lake, Abraham, 45 Lake, Abraham, 63 Lake, Abraham,
100 Lake, Abraham, 258 Lake, Abraham Wright, 100 Lake, Abraham
Wright, 2d, 100 Lake, Ada, 27 Lake, Adelaide S., 154 Lake, Aeltie, 20
Lake, Aeltie (Burbank), 20 Lake, Aeltie (Burbank), 21 Lake, Agatha,
168 Lake, Agnes, 144 Lake, Agnes Kearney, 230 Lake, Agnes
Livingston, 17 Lake, Ailse, 26 Lake, Albert Bowen, 141 Lake, Albert
P., 141 Lake, Alberta, 155 Lake, Alberta, 226 Lake, Alberta, 246
Lake, Alee (Stillwell), 18 Lake, Aletta Ann, 15 Lake, Alexander, 48
Lake, Alexander, 65 Lake, Alfred Warren, 208 Lake, Alice, 19 Lake,
Alice E. (Core), 127 Lake, Alida, 21 Lake, Alleday, 20 Lake, Allen, 58
Lake, Almira C, 88 Lake, Alwilda, 61 Lake, Alwilda, 88 Lake, Amanda
(Adams), 118 Lake, Amanda B., 96 Lake, Amanda E. (King), 142
Lake, Amariah, 40 Lake, Amariah, 52 Lake, Amariah, 147 Lake,
Amariah, 203 Lake, Amariah, 260 Lake, Amelia, 232 Lake, Amy
(Gordanier), 27 Lake, Andrew, 42 Lake, Andrew, 45 Lake, Andrew,
56 Lake, Andrew, 88 Lake, Andrew, 259 Lake, Ann, 3, 12 Lake, Ann,
19 Lake, Ann, 22
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