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OSTEITIS OR SKULL OSTEOMYELITIS:
INCIDENCE WITHIN A FLORIDIAN SAMPLE
A Thesis
Presented to
The Faculty of College of Arts and Sciences
Florida Gulf Coast University
In partial fulfillment
of the requirement for the Degree of
Masters of Science
By
Kreshlya De La Paz Rodriguez
2015
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TABLE OF CONTENTS
ACKNOWLEDGEMENTS ………………………………………………………………….4–5
ABSTRACT…………………………………………………………………………………...6–7
CHAPTER ONE: INTRODUCTION……………………………………………………….8-14
CHAPTER TWO: SKELETAL PATHOLOGIES ………………………………………15–20
CHAPTER THREE: DIFFERENTIAL DIAGNOSIS…………………………………...21–27
CHAPTER FOUR: MATERIALS………………………………………………………...28–32
Inventory…………………………………………………………………………………29
Demographics….………………………………………………………………………...29
Skeletal Age Estimation…………………………………………………………...…30–31
Sex Assessment…………………………………………………………………………..31
Ancestry Assessment…………………………………………………………………….32
CHAPTER FIVE: PROCEDURES……………………………………………………….33–36
Skull Osteomyelitis or Osteitis………………………………………………………33–34
Otitis Media……………………………………………………………………………...34
Auditory Exostoses………………………………………………………………………35
Cholesteatomas…………………………………………………………………………..35
Cribra Orbitalia and Porotic Hyperostosis……………………………………………...35
Linear Enamel Hypoplasia…………………………………………………………...35–36
Periodontal Disease………………………………………………………………………36
Dental Abscess…………………………………………………………………………...36
CHAPTER SIX: RESULTS………………………………………………………………..37–40
CHAPTER SEVEN: DISCUSSION…………………………………………………….....41–46
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CONCLUSION…………………………………………………………………………………47
APPENDIX A……………………………………………………………………………….48–60
APPENDIX B……………………………………………………………………………….61–67
REFERENCES……………………………………………………………………………...68–73
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ACKNOWLEDGEMENTS
First and foremost, I dedicate this work to my parents and grandparents. They are my
angels and without their trust and support I would not have been able to finish my degree. I give
special thanks to my mentor and thesis Chair Dr. Heather Walsh-Haney. She is an extremely
dedicated person that works for the well-being of all her students while becoming more than just
a mentor, she became a friend. I cannot thank her enough for accepting me and providing me the
opportunity to join her graduate program. Most of all I thank her for her support and trust during
the course of this study. I thank Dr. Mary Ann Zager for her statistical explanations, support and
great advice. I am grateful for Dr. Manfred Borges’s anatomy lessons, Socratic questions, and for
being part of my thesis committee. I could not have asked for a better statistics and thesis
advisors.
I also thank Dr. Marta Coburn for her thorough critique of my findings and the time she
took to help me develop the differential diagnosis. I will never forget the conversation we had
which helped me to grow as a student and as a person. I thank Dr. Phoebe R. Stubblefield for her
comments and recommendations regarding my analysis process. Her insight clarified many of
my doubts and made me realize the greatness and potential of this study. No less important, I
thank Dr. Susan Antón for taking time to analyze some of the remains and sharing with us her
thoughts and concerns. Without her help and emails, we would not have completed this study.
I am in debt with the staff of Collier and Palm Beach County Office of the Medical
Examiners’ Offices. I thank them for opening the doors of their offices to me; offering me a
space to conduct my analysis; lending me instruments; and allowing me to analyze skeletal
remains with the understanding that I would be adding information to previous analyses.
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I give special thanks to my niece—thanks for just being you—my “Minimi”. I thank my
good friends Ms. Paloma Martinez, Ms. Nilka Marie Rodriguez, and Ms. Samantha Wade for
listening and helping me throughout my master’s degree. Each one of you motivated me to finish
this thesis and I will never forget you. I thank all of my family members and friends for their
encouragement which helped me to never give up.
Lastly, I thank Mr. Antonio Marques for being the person that helped me the most during
these last three years. More than my boyfriend, he is my best friend. Without his support my
Master’s degree would not be conferred. I especially thank Antonio for reading and re-reading
every one of my papers. Thanks for your patience, visits and comments; for making me feel that
I was not alone; for all your love. Thank you, miamor…
-Ms. Kreshlya De La Paz Rodriguez
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Abstract of Thesis Presented to the Graduate School
of Florida Gulf Coast University in Partial Fulfillment of the
Requirements for the Degree of Master of Science
OSTEITIS OR SKULL OSTEOMYELITIS:
INCIDENCE WITHIN A FLORIDIAN SAMPLE
By
Kreshlya De La Paz Rodriguez
May 2015
Chair: Heather Walsh- Haney
Major Department: Forensic Studies
This study examines the occurrence of skull osteomyelitis/osteitis using four samples
from modern Floridian contexts. The aim of this research was to develop a new method of
identification for skull osteomyelitis/osteitis as well as, identify its etiology and demographics.
For etiology purposes, I examined the co-occurrence between of skull osteomyelitis/osteitis and
eight additional cranial pathologies: otitis media, cribra orbitalia, auditory exostoses,
cholesteatoma, porotic hyperostosis, linear enamel hypoplasia, periodontal disease, and dental
abscesses. I evaluated the location, depth, and extent of granulation erosion and scored the
lesions as present or absent.
Overall, the most common bone with evidence of skull osteomyelitis/osteitis lesions was
the frontal bone followed by (in descending rate of occurrence) the temporal, parietal and
sphenoid bone. This condition favored males over females which was consistent with previous
clinical studies. However, this analysis diverged from the previous research with the age of
individuals with the condition tending to be less than 60 years (median age range = 32–62 years).
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Periodontal disease was the most common disease to co-occur skull osteomyelitis/osteitis which
was contrary to previous research in which otitis media held that distinction.
A total of 40 (33%) individuals exhibited skull osteomyelitis/osteitis. This result
illustrates that skull osteomyelitis/osteitis might not be a rare condition as published by other
researchers. Furthermore, this sample comprises individuals from all ancestry groups, both
biological sexes and different ages unlike previous research that comprised mostly geriatric
European males.
The etiology of skull osteomyelitis or osteitis is inconclusive although, this study
supports the designation as a nonspecific bone infection. This study, however, shows the
condition can be triggered by six different disease processes that originate in the venous or sinus
systems. Skull osteomyelitis is an infection within the bone marrow whereas osteitis is a
generalized bone inflammation that can affect and/or destroy any compact bone structure
Therefore, instead of labeling this condition as skull osteomyelitis I concluded that the lytic
lesions were mostly related to osteitis rather than osteomyelitis.
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CHAPTER ONE
INTRODUCTION
Throughout history, different cultures around the world have studied the human body in
an attempt to understand its complexity. Aside from the brain and genetic code, which scientists
are constantly examining from different angles, human anatomy has become a well-studied
subject within the scientific community. The skeletal system lends itself to a plethora of study
modalities because it is a living and rigid structure responsible for muscle support, protection of
vital organs, movement, blood manufacturing, and storage of essential vitamins and minerals.
For example, biological anthropologists, bioarchaeologists, and skeletal anatomists study bone
on a microscopic level to interpret cranial trauma (Boldsen et al. 2015); a macroscopic level to
reveal the epidemiology of osteoporosis (Curate 2014); use computer methods to understand the
biomechanical causes of rib fractures (Cai et al. 2015), respectively. No matter the level of
analysis (microscopic, macroscopic, radiographic, elemental, etc.) the observer implicitly records
his/her observations on a cellular level by intrinsically evaluating the ratio of osteoblastic to
osteoclastic change.
Osteoblasts and osteoclasts are the bone cells responsible for the formation (a blastic
response or bone cell deposition) and resorption (a lytic response or bone cell destruction) of
skeletal tissue, respectively. These cells create two basic skeletal structures: compact and spongy
bone (Hansen, 2002, White, 2012). The compact, cortical or lamellar bone comprises the
external structure that creates the walls of the bone shafts as well as the joint surfaces. The
spongy or trabecular bone is a highly vascularized structure found inside the vertebral bodies,
within the ends of the long bones, short bones, and flat bones (White, 2012; Ortner, 2003). Due
to its basic architecture, compact bone is not nourished by the nearby blood vessels; therefore,
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compact bone acquires nutrition from two different blood and lymph pathways: the Harvesian
(vertical) and Volkmann (horizontal) canals. In life, the outer surfaces of the compact bones are
covered with a thin, vascularized tissue layer known as the periosteum. A cellular layer known as
the endosteum covers the internal bone structures shaped by the trabecular bone. The cranium,
unlike most of the postcranial bones, is arranged with two layers of compact bone separated by a
layer of trabecular bone known as diploë (White, 2010).
Bone appears to be a closed system because it is encased within the dermis, skeletal
muscle, fascia and the periosteum. However, the skeletal system is actually an open system
because, bacterial and other infections can reach the bone’s compact or trabecular structures via
hematopoietic pathways. For example, osteitis is a generalized bone inflammation that occurs
when pathogens on the outside of the skeleton find their way into the cortical bone (White,
2010). Osteitis may first be observed by the patient or clinician when the body’s reaction to
infection manifests as a site of pain, swelling or both. When clinically diagnosing otitis media,
for example, the physician may observe a generalized inflammation of the pinna of the ear that
may later develop into a bacterial infection that erodes the compact bone of the temporal
(Ruuskanen, 1994; Ortner, 2003; White, 2012). In contrast, osteomyelitis is an infection that
begins in the bone (osteo) marrow (myelo) affecting the endosteum, Harvesian system, and
periosteum (Ortner, 2003; Pincus, 2009). White (2012), a paleoanthropologist, adds to this
definition by indicating that osteomyelitis is an osteological condition caused by a pus-producing
microorganism that reaches the bone as a result of an injury or via the bloodstream. Kim (2012)
also states that the inflammatory process of osteomyelitis occurs along with bone destruction. In
general, osteomyelitis is most often observed within a long bone where the pus-producing
microorganism induces the clastic response in the cortical bone through the creation of holes or
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cloaca that allows the exudate to drain (Ortner, 2003). The condition generally develops
secondary to a bacterial infection (Staphylococcus aureus or Pseudomonas aeruginosa), fungal
infection, trauma, or postoperative surgery (Pincus, 2009; White, 2012).
Compared to the postcranial skeleton, osteomyelitis infections within the skull are
considered rare (Blyth, 2010; Chandler, 1986; Chang, 2003; Leventhal, 2011; Pincus, 2009;
Ortner, 2003). Blyth (2010) explains that the condition is considered uncommon based on the
results of an 18-year retrospective study (1990-2007) in which cases were identified following
the examination of medical records from the International Statistical Classification of Diseases
and Related Health Problems definitions, 10th revision, Australian modification. In this study, 21
out of 500 patients from the Westmead Hospital were diagnosed with osteomyelitis of the skull.
Chandler (1986) stated that if reported, this condition typically resulted from an
uncontrolled middle ear infection, i.e., malignant otitis externa, caused by the P. aeruginosa
bacteria. This bacteria gains access via the soft tissue and if untreated will eventually progress
until it reaches the temporal bone (Blyth, 2010; Chandler, 1986; Chandler, 1989; Kim, 2012.;
Mahdyoun, 2013; Singh, 2005). Besides damaging the petrous portion of the temporal bone, this
condition may also advance into the sphenoid and occipital bone, via the venous (or venous
sinus) system. Thus, the expectation became that the frontal and parietals bones should lack the
hallmarks from the condition, such as cloaca, lytic lesions, necrotic lesion, etc. Chandler (1986)
described the average patient with osteomyelitis of the skull as elderly, diabetic, and male. He
observed that the condition affected the bones of the cranial base (i.e., occipital, sphenoid,
temporal) and identified the condition as skull-base osteomyelitis. His findings were biased,
however, because he focused upon a hospital sample (Wood et al. 1992). Furthermore, other 21st
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century researchers observed that the condition also affected the frontal, sphenoid, ethmoid and
maxillae by way of the paranasal sinuses.
Previous researchers have reported cases in which skull-base osteomyelitis typically
emerged from paranasal infections, instead of ear infections (Blyth, 2010; Chang, 2003;
Enriquez- Santos, 2010; Magnulio, 2000; Pincus, 2009). Chang (2003) studied six male patients
(with a mean age of 40 years) that developed skull-base osteomyelitis from a sphenoid sinus
infection triggered by an Aspergillums fungus. This finding was consistent with Furstenberg’s
(1934) study that indicated that the spread of osteomyelitis was also associated with
complications due to insufficient sinus drainage from which the reminder of the primary bacteria
extended into the sinuses and orbits. Similarly, Magnulio (2000) recognized that the role of the
maxillary (and mandibular) sinuses pay as a vector for skull osteomyelitis. To wit, Magnulio
found that maxillary and mandibular caries (or cavities) can prompt the manifestation of the
condition because of the interconnectedness of the tooth and bone tissues. Moreover, patients
with dental extractions, periodontal disease, multiple myeloma or metastatic bone cancer have
high risks of developing the condition due to their compromised blood and immune systems
(Reilly, 2007). In other words, these researchers agree that any bacteria within the blood vessels
can affect the cranial blood supply resulting in skull-base osteomyelitis (Furstenberg, 1934;
Levanthal, 2011). The resultant bony lytic lesions would follow the path of the arterial and
venous channels in the cranium marking the inner table first and if not treated then proceeding to
the outer table (Furstenberg, 1934).
Cranial fractures and osteonecrosis (bone death) of the mandible are also plausible causes
of skull osteomyelitis. One clinical study which followed bisphosphonate treatments used to
prevent the loss of bone mass noted that osteomyelitis tended to manifest after the course of
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treatment. The connection between the treatment and osteomyelitis underscored that the body
responded to an imbalance in osteoblastic deposition and osteoclastic resorption (Reilly, 2007).
For example, when the levels of bone resorption (the clastic response) were higher than those of
bone deposition (the blastic response), the bone became weak, cavernous and primed for
bacterial infections. The osteomyelitis locations for these studies do not tend to predilect the
bones of the skull base; therefore, in terms of identifying general inflammation within the bone
secondary to an infection—such as skull osteomyelitis or osteitis—tend to be considered more
apropos. Nevertheless, at least one 21st researcher has data supporting Chandler’s findings as
well as his nomenclature.
Blyth’s (2010) retrospective study of skull-base osteomyelitis found similar results as
those from Chandler’s study (1986). Yet, Blyth showed that if skull-base osteomyelitis arises
from a fungal infection the condition advances at a faster pace especially when compared to
infections that were bacterial, traumatic, postoperative, or from the P. aeruginosa strain.
Following Chandler’s (1989) and Blyth’s (2010) findings that skull-base osteomyelitis is
a rare condition affecting old-aged, diabetic males with chronic middle ear infections, I
examined four contemporary skeletal collections from the state of Florida for evidence of skullbase osteomyelitis, skull osteomyelitis or osteitis as markers of generalized skeletal
inflammation. Since osteitis is an inflammation that affects the compact bone, I considered this
condition as a possible explanation for lytic lesions within the inner table of the cranium. In
addition, I use the term skull osteomyelitis, instead of skull-base osteomyelitis, in recognition
that the condition may affect all of the bones of the skull not just the bones of the base (occipital,
sphenoid, and temporal).
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The collections under study contained the skeletal remains of modern individuals from
both biological sexes and different ages—a sample contrasts with the previous studies that
comprised mostly geriatric males. In addition, I evaluated all ancestry groups present, i.e., Asian,
European, and African which diverges from the previous studies that focused upon European
groups. My samples provided me the opportunity to hypothesize that (1) the frequency of
occurrence of skull osteomyelitis and/or osteitis would be greater within the male sample than
female sample, and (2) the frequency of individuals with skull osteomyelitis/osteitis will be
greatest among old-aged (65+ years) individuals.
To understand the possible connection between skull osteomyelitis or osteitis with other
pathological conditions (i.e., bacterial, fungal, or teeth infections) I examined eight (8) additional
skull pathologies that have been linked to blood system disorders and can be identified via visual
(macroscopic) examination of the bones. First, I analyzed infections related to malnutrition,
genetic disorders, stress, or blood deficiencies, such as cribra orbitalia, porotic hyperostosis, and
linear enamel hypoplasia. Secondly, I analyzed the temporal bone for evidence of lytic lesions,
auditory exostosis, and cholesteatomas. Lastly, I examined the remains for evidence of
periodontal disease and dental abscess because these conditions have been linked to paranasal
sinuses infections or are blood conduits into the cranium. My assumption was that the frequency
of co-occurrence of skull osteomyelitis or osteitis with cribra orbitalia, porotic hyperostosis,
linear enamel hypoplasia, otitis media, auditory exostoses, cholesteatoma, periodontal disease,
and dental abscesses would not be equal to the mean numbers of pathologies per individual.
This research project is of significant importance within the medical and forensic fields
because clinicians and pathologists may be relying too heavily upon biased data (e.g., Chandler,
1986) that report the incidence of skull-base osteomyelitis as rare. By extension, the medical and
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forensic community may not expect to encounter the condition and disregard skull osteomyelitis
or osteitis as the condition related to a patient or subject’s death and/or fail to identify bacterial
or fungal geographic hot spots of community health importance.
This thesis is also important because it builds upon my pilot study which I presented at
the American Association of Physical Anthropology meetings (De La Paz, 2014), entitled
“There’s a hole in my skull dear Liza: Skull-based osteomyelitis”. For the pilot study, I
investigated the two hypotheses listed above with a sample that included fourteen (14) skeletal
remains exhibiting lytic lesions associated with skull-base osteomyelitis. Based upon my
preliminary findings (the presence of one middle-aged female with the condition but absent
petrous pyramid lytic lesions), I decided to expand my study and examine a larger sample.
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CHAPTER TWO
SKELETAL PATHOLOGIES
The human skull is a complex assemblage of bones that form one complete super-arching
structure united by sutures. For example, seven bones are connected to create the human orbit
(i.e., frontal, zygomatic, maxilla, sphenoid, ethmoid, palatine, and lacrimal). In addition, there
are multiple foramina that serve as continuous passageways for veins, arteries and nerves to
carry blood, oxygen, nutrients, and neurons from the skull to the postcranial skeleton and back
again. Cavernous areas or sinuses hold or transport blood, air and mucosa. However, these
hollow passages and empty spaces can also serve as conduits or homes for infections causing
bacteria.
Skull osteomyelitis and/or osteitis are conditions that develop secondary to many other
disorders including those that are traumatic or pathologic in nature. Therefore, understanding the
etiology of skull osteomyelitis/osteitis (be it bacterial or fungal) and the skeletal routes infections
may take the skeletal analyst to identify abnormalities and the clinician to treat or prevent illness.
A discussion of skull osteomyelitis or osteitis would not be complete without documenting the
various primary pathologies that tend to give rise to the condition.
Pathogenesis and the Ear
According to Chandler (1986) skull-base osteomyelitis tends to stem from the clinical
diagnosis of otitis media. Daniel (1988) defines otitis media as the abnormal accumulation of
fluid within the middle ear (e.g., the bony space within the temporal that includes three
ossicles—incus, malleus, and stapes—that runs from the tympanic membrane to the oval window
of the petrous pyramid) caused by an infection (bacteria) that requires antibiotics or surgery. If
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left untreated the condition can advance into meningitis, mastoiditis, tympanic membrane
rupture, or a cholesteatoma (see below). Daniel (1988) also noted Native Americans and Inuits
were more likely to exhibit this condition due to their large Eustachian tubes (ET) as compared
to Europeans. Daniel proposed the difference in ET anatomy made Europeans more likely to
develop cholesteatomas from untreated otitis media. Ruuskanen (1994) identified the
pathogenesis of otitis media’s by noting that children tended to manifest the condition when
bacteria, usually Pseudomonas aeruginosa or Staphylococcus aureus, from the respiratory track
reached the middle ear. There the bacteria would remain for weeks to months and would
eventually lead to draining, malodorous exudate and cholesteatomas.
Relatedly, forensic anthropologist Dr. William Maples helped to positively identify
skeletal remains when he identified a middle ear infection as evidenced by the presence of lytic
lesions of the temporal bone consistent with otitis media that he believed induced a
cholesteatoma (Maples, 1994; Wade, 2013). Maples went on to describe that the decedent
probably had hearing problems, nerve problems and/or suffered from disorientation. Iino (1998)
studied thirty-four (34) cases of cholesteatomas and documented that there are two types of
cholesteatomas. The first or One-Type Cholesteatoma is likely to be congenital and caused by
continuous epidermoid formations. The second or Close-Type Cholesteatoma is formed by a cyst
(dead keratinized epithelial cells) that is usually a consequence of small or absent mastoid air
cells, which accelerates inner ear inflammations and causes otitis media. Mays (2006) explained
that that One-Type Cholesteatoma is also known as External Canal Cholesteatomas (ECC) while
Close-Type Cholesteatomas are identified as Middle Ear Cholesteatomas (MEC). The middle
ear, however, is not the only part of the temporal bone that gives rise to ear infections.
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Auditory exostosis is identified as a pathological condition that affects the auricle (i.e.,
the ear canal and external margin of the external auditory meatus (EAM) of the temporal). This
condition predilects males and is evidenced by the bony projections or outgrowths around the
EAM (Hrdlicka in Hutchison 1997). Different researchers have published that the main
stimulating factor for this abnormal bone growth is cold water. Nonetheless, Hutchison (1997)
did a histology study of these bony projections and his results indicated that the projections were
layers of compact bone caused by otitis externa, i.e., an ear infection in the EAM triggered by an
imbalance of pH levels in the area around the auditory canal. Hutchinson’s sample comprised
individuals whose lifeways revolved around swimming and diving to acquire marine resources.
Although otitis externa is associated with water and bacteria, Hutchison advocated that the
infections arose from bacteria not the accumulation of water in the ear canal.
In order to clarify the causes of auditory exostoses, Godde (2010) analyzed a population
which had little or no exposure to bodies of water. In her data, four (4) out of seven hundred
forty-four (744) individuals were positively identified with the condition. Thus, the author
concluded that there must be other possible factors or conditions that provoke exostoses around
the (EAM) such as systemic conditions or a genetic predisposition.
Pathogenesis and Hematopoiesis
Skull osteomyelitis or osteitis may be the consequence of blood disorders that arise from
malnutrition, genetic mutation, trauma or myriad diseases. For example, cribra orbitalia and
porotic hyperostosis are pathological conditions associated with an iron deficient diet (e.g., iron
deficiency anemia). As a result, the hematopoietic marrow of the affected bones expands and
reabsorbs the outer table, leaving the trabecular bone exposed (White, 2012; Ortner 2003; Stuart-
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Macadem, 1985). Cribra orbitalia marks the orbital roofs of the frontal bone whereas porotic
hyperostosis tends to affect the parietal and occipital bones (and to a lesser extent the sphenoid,
temporal and frontal). Even though it is scientifically recognized that the porotic appearance on
the orbital roofs and external surface of the parietals are due to bone expansion, other researchers
have argued that the porosity of the bones can also be a consequence of the healing process
(Ortner, 2003). In addition, other conditions such as rickets, genetic disorders, or brain tumors
can be responsible for the coral-like appearance of these two conditions.
Walker (2009) analyzed the different theories about the etiology of cribra orbitalia and
porotic hyperostosis and realized that the first studies of both conditions were completed with
skeletal remains of individuals from developing countries and then on Native American remains.
Both populations’ diets were corn based (a vegetable related to iron-deficiency) which
bioarchaeologists linked the cranial evidence to an iron deficiency anemia. However, anemia
(deficiency of red blood cells) can also arise from a lack of gastrointestinal iron absorption. An
iron deficiency impedes hemoglobin synthesis and red blood cells (RBC) from maturing;
therefore, it cannot be responsible for the osseous expansion of the cranial vault. Walker
concludes that the abnormal spongy appearance of the inner and outer tables is more likely a
consequence of a deficiency in vitamin B12 rather than a consequence of an iron deficiency.
Ortner (2003) also suggests that cribra orbitalia and porotic hyperostosis should not be a linked
to a specific condition, like anemia. Rather, Ortner underscores that cribra orbitalia and porotic
hyperostoses are the symptoms of multiple conditions.
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Pathogenesis and the Mouth
In the same manner that an individual’s cranial vault is affected by malnutrition and other
disorders, teeth can also be marked by the same stresses. For example, normally tooth enamel
begins to form from the crown and ends with the formation of the tooth root. Yet, childhood
metabolic disorders can alter the process of amelogenesis (enamel formation) causing disruption
of the enamel (Ortner, 2003). Hypoplastic lines are the transverse lines or grooves on the tooth’s
enamel caused by systemic physiological stresses such as poor nutrition, traumatic injury, or
illness (Martin, 2008; White, 2012.) The development of these lines can also be affected by
conditions such as congenital syphilis, tuberculosis, rickets, or endocrine syndromes (Ortner,
2003). Enamel disruption is pathologically identified as linear enamel hypoplasia (LEH). The
presence of LEH has been an extremely useful tool for skeletal analysts when evaluating overall
health status in children.
An individual’s dentition can also be disturbed by bacterial invasion. Gingivitis is an
“inflammation of the soft tissue that surrounds teeth, usually at the junction between the dental
crown and root” (Ortner, 2003; p.593). If untreated this condition develops into a periodontitis or
periodontal disease which is a deep inflammation that causes loss of the soft tissue and alveolar
bone and creates soft pockets of infected tissue between the gum (gingiva) and teeth (Pihlstrom,
2005). Over the last few decades personal oral hygiene has greatly improved and nowadays more
individuals have access to dentists. Nevertheless, periodontal disease is still very common and
tends to affect more males than females as well as individuals of low socioeconomic status.
Genetics and pathological conditions such as malnutrition, alcohol and tobacco use, osteoporosis,
and diabetes can prompt periodontitis (Pihlstrom, 2005; Teng, 2002). Respiratory bacterial
pathogens like Pseudomonas aeruginosas and/or Staphylococcus aureus have been linked to
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periodontal disease (Teng, 2002). In dry bone, periodontal disease is evident when there is a loss
of the alveolar margin and teeth are loose although still present. Also the lack of dental caries,
e.g., bacterial infections that destroy the structure of teeth, with well-defined alveolar bone loss is
indicative of periodontal disease (Ortner, 2003.)
Dental caries is an infectious and transmissible disease in which microbial activity
(usually Streptococcus mutans with other bacteria) progressively destroys the tooth crown and
root. If untreated, the root becomes exposed leading to a sequelae abscess and destruction of the
adjacent bone. White (2012) describes dental abscesses as the localized collection of pus formed
by tissue disintegration that may be periapical (most commonly involving the tip or apex of the
tooth root) and can accelerate into a meningitis, brain abscess or hematogenous (skull)
osteomyelitis (Ortner, 2003). Dental abscesses are secondary outcomes of caries or trauma, but
in rare cases can also arise from a botched root canal or dental fillings; hence, bacteria cultivates
within the root canal or filling and gains access to the bone’s tissue through the apical foramen
and spreads the infection (Shweta, 2013).
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CHAPTER THREE
DIFFERENTIAL DIAGNOSES
Human identity and trauma analysis is a field within forensic science that requires years
of experience and knowledge of the human body and its anatomy. Osteologists, biological
anthropologists, bioarchaeologists, and forensic anthropologists are the experts focused on
identifying if the skeletal element under examination was affected by trauma or change induced
by biological or environmental variables as well as differentiating the anomalies from normal
human anatomy. The analysis of skeletal remains involves a deep understanding of the different
types of trauma, i.e., any signs of osteological changes, as well as the skeletal response to the
trauma itself. White (2012) describes the biological process that results in skeletal trauma as:
antemortem changes, i.e., those skeletal modifications that happened in-life; perimortem
changes, i.e., cultural practices which took place around or at the time of death; postmortem
changes, i.e., changes to the bone that occurred after death. Biological processes, such as
diseases and genetic disorders, are classified as antemortem changes. In dry bone, a skeletal
analyst can try to identify if the individual suffered from a disease by evaluating the
macroscopic, microscopic, radiographic and elemental condition of the bone. However,
differentiating between ante-, peri-, and postmortem change is not clear-cut.
As a case in point, skull osteomyelitis or osteitis and arachnoid (or granular) fovea are
both identified as holes within the endocranial surface of the vault. However, arachnoid
granulations are round and tend to be centered along the coronal suture and are rarely seen within
or along the transverse sinus of the occipital (Pacchioni, 1741 in Turner, 2008; Duray 2006). The
arachnoid granulations form as extensions of the pia-arachnoid tissue, i.e., two of the meningeal
layers that cover the brain, and spinal cord as they push their way through the inner table (Duray,
2006; Turner, 2008). Esposito (2011) explains that these granulations are a result of an
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invagination of the dura floor that creates bone resorption of the inner table. They are relatively
small in size and if visible (by the naked eye) are known as Pacchionian Granulations (PG).
Furthermore, PG do not contain blood vessels; rather, their purpose is to absorb cerebrospinal
fluid (CSF) and drain the fluid into the venous sinus system. Previous studies have shown that
PG size increases with age. Furthermore, as a person ages the possibilities of finding larger PG
increases (Bastian, 1866; Esposito, 2011). Nonetheless, Duray (2006) conducted a study
intended to analyze the volume of arachnoid granulations and the results demonstrated that the
size of the granulation is more closely associated with the individual’s health status than his/her
actual chronological age. Esposito (2011) also studied giant granulations and concluded that
these granulations are filled with CSF caused by intracranial pressure and otitis media and are
more likely to be found in the anterior and middle cranial fossa.
In order to determine the specific etiology and differentiate normal anatomy (PG) from
serious skeletal pathology (skull osteomyelitis or osteitis) contextual clues (demographics,
topographical, historical) must be considered. However, in most forensic anthropology settings
this information is unknown.
Wood (1992) explains that the paradox in understanding health status from skeletal
samples is far more than just examining the skeletal remains; rather, he stresses that the skeletal
analyst must understand the demography, mortality, and heterogeneity of the study sample in
order to correctly interpret the findings. While Wood focused upon cemetery, historic and prehistoric samples, Kaufman (1997) added another caveat to Wood’s osteological paradox—that a
complete diagnosis of contemporary skeletal remains must include: (1) the clinical history of the
decedent, (2) histological sections of the lesion, and (3) modern clinical data and radiographic
22
studies. In addition, this author explains that a proper diagnosis cannot be accomplished without
analyzing the complete skeleton.
Pathological conditions can present similar appearances and symptoms; therefore,
differentiating one disease from another is essential. Osteitis is prompted by an infection that can
affect and/or destroy any compact bone structure within the skeleton (White, 2012). It may affect
males and females at any moment during their lives. Osteomas are benign, solitary and round
projections of bone that tend to be found on the outer table of the cranial vault. They are easily
distinguished from osteitis because the abnormal bone formation is subperiosteal (Ortner, 2003;
White, 2012). Similarly, osteoid osteomas and osteoblastomas are differentiated from osteitis
because the lesions comprise round, dense lamellar (blastic) bone and are usually found on the
appendicular skeleton of teenagers or young adults. Osteomas typically marked the long bones
and tarsals while osteoblastomas predi,lect in the vertebral bodies, hands, and feet (Ortner,
2003).
Osteosarcomas and osteochondromas tend to arise in the growth plate of the longer
extremities (humerus, radii, ulnae, femora, tibiae, fibulae) instead of the cranium (White, 2012;
Ortner, 2003). Osteosarcomas are most commonly seen in young children whereas,
osteochondromas affect older adults. The abnormal cartilage production around the metaphysis
of the long bones differentiates these conditions from osteitis.
The bony lesions associated with osteitis and hemangiomas are tethered to the body’s
blood supply in order to proliferate. However, hemangiomas are extremely rare (12.2%
occurrence for males and 15.9% for females over 60 years) and tend to affect the vertebrae and
in rarer cases the cranium. This condition replaces the bone’s hematopoietic marrow with a
mixture of blood and fat cells which causes a distortion in the marrow’s balance and reduces the
23
number of vertical trabeculae. In the diploë, these lesions appear roundish in shape and destroy
the inner and outer tables—just as in osteitis. However, the pathologies may be parsed by the
radial arrangement of the diploë seen with hemangiomas (Ortner, 2003).
Similar to a hemangioma tumor, a meningioma tumor invades the cranium through the
inner table and produces lytic and blastic lesions. The lesions may appear as bone spicules and
destroys the outer table (Ortner, 2003). Because skull osteomyelitis and osteitis rarely produce
bone spicules they can be differentiated from a meningioma.
Paget’s disease, also known as osteitis deformans, is a condition commonly found in
European males over forty (40) years-old. Ortner (2003) defines this condition as one in which
the affected bone becomes warped and enlarged due to an imbalance in osteoblast production
and osteoclast resorption. At first, incessant osteoclastic (destruction) activity occurs and is
followed by an unstoppable osteoblastic activity (remodeling). The first stage in the skull
involves the (lytic or destructive) resorption of the diploë. Subsequently, the cranium enters into
a remodeling process that creates thick cranial walls. Paget’s disease can be differentiated from
osteitis and skull osteomyelitis due to the fact that while Paget’s goes through a lytic stage the
diseased skull will bear some evidence of abnormal widening and enlargement.
Treponema pallidum pallidum, also known as venereal or acquired syphilis, is one of the
four different syndromes from the Treponemal family that affects humans by entering the body
through abnormal or normal breaks in the skin as well as the mucous membranes (White, 2012).
If sexually acquired, the infection moves through three stages with bone deterioration beginning
in the tertiary stage (about 2–10 years after contracting the disease). The disease first marks the
outer table of the frontal bone and subsequently involves the parietal and facial bones. The
granulations are accompanied by an osteoblastic or remodeling process of the outer table and
24
diploë. The inner table is rarely impacted. The large scale of the cranial lytic foci in the outer
table impedes a uniformed and smooth remodeling process; thus, scars (which are usually round
or stellate in shape until they coalesce) are visible even after the remodeling process. Therefore,
the condition is easily discernable from osteitis.
Tuberculosis is an infectious disease caused by the bacterium Mycobacterium
tuberculosis. While the last few decades have been associated with a decrease in the disease,
recent years have evidenced an increase in the condition with HIV and migration being
contributing variables within the western parts of Asia and other developing countries (Pan,
2014, White 2012). Skull lesions are rarely observed with tuberculosis. Rather, the condition
commonly manifest within the vertebral bodies. However, the condition has been observed
within the skulls of young children typically from Africa and Europe. Tuberculosis is considered
more as an endemic condition in which children become exposed by being in contact with
infected family members. When present in children, the lesions are round and perforate both
cranial tables. In addition, the lesions do not cross suture lines, but they do produce cranial
abscesses (Ortner, 2003). Because the condition tends to affect the skulls of children combined
with the fact the lesions cross both cranial tables, tuberculosis can be differentiated from osteitis.
Multiple myeloma is a malignant disorder of the plasma cells that affects the bone
marrow and induces abnormal osteoclastic activity (Rothschild, 1998; Joshi et al, 2011). The
common patients are 50+ year-old males who present with bone pain, osteopenia, and lytic
lesions that predilect the axial skeleton. In the first stage, the tumor starts with a solitary lytic
lesion that after a while can incite the process of bone remodeling (Ortner, 2003). By genetically
inducing abnormal osteoclastic activity the formation of new bone cells is also hindered; hence,
the multiple punched-out lytic defects may mark the entire skeleton (Rothschild, 1998;
25
Roodman, 1997). In the skull, the myeloma lesions penetrate both tables, lack smooth borders,
and range between 2–5mm in diameter (Rothschild, 1998; Ortner, 2003). In addition, the lesions
appear as circular or enlongated depressions (Rothschild, 1998). Myloma lesions are easily
differentiate from osteitis since the myeloma lesions cross both cranial tables and are larger in
diameter.
The process of differential diagnosis became more difficult when assessing cancers such
as breast or prostate which also affect the skull when they metastasize and become metastatic
cancer (MC). For example, in the skull, Rothschild (1998) explains that the lytic lesions
normally associated with metastatic cancer are elliptical with residues of a cortical shell and bone
trabeculae that resemble the surface of a golf ball (p.241). In addition, these lytic lesions have
irregular borders which are associated with reactive bone disease (Ortner, 2003). Although, MC
produces residues of a cortical shell and/or destroys the inner and outer table; the fact the
individual may die from a secondary condition (like a gunshot wound) when only one focal
lesion is present, make the differentiation of these conditions difficult. As such, in some
instances the metastatic cancer cannot be ruled out as a probable diagnosis. Interestingly,
because MC is not linked to a specific biological sex or age range and skull osteomyelitis tends
to be found in geriatric males according to Chandler (1986) and Blyth (2010), demographic
information will help differentiate MC from skull osteomyelitis.
The last condition considered for differential diagnosis is Langerhans Cell Histiocytosis
or (Histiocytosis X). Histiocytes are macrophages responsible for the removal of abnormal or
dead cells. These cells manifest in three different ways: unifocal Langerhans Cell Histiocytosis
(LCH) (e.g., eosinophilic granuloma), multifocal unisystem LCH (e.g., Hand-Schüller-Christian
disease), and multifocal multisystem LCH (e.g., Letterer-Siwe disease) (White, 2012). The last
26
manifestation, (multifocal multisystem LCH), occurs in children under the age of three (3) years,
while Hand-Schüller-Christian disease affects children, adolescents and young adults with a
predilection for children less than five (5) years-old. Eusinophilic granuloma develops in
children and also young adults. The three different manifestations of the disease affect the
cranial vault (orbits, parietals, and sphenoid) and base (occipital) with one or multiple lytic
lesions (Ortner, 2003). The lesions are oval with beveled margins that lack reactive bone
formation. However, the lesions associated with Hand-Schüller-Christian disease are multiple,
large in size and in some cases merged to each other (Ortner, 2003; White, 2012). The age
demographics of HTC (mostly affects children) and diameter of the lesions will aid to
differentiate this condition from osteitis or skull osteomyelitis.
Based upon the demography as well as lesion description and location, arachnoid
granulations may not be easily ruled out when differentiating between those granulations and
osteomyelitis or osteitis. Appendix A (Figure 3.1) presents an analytical diagram that
summarizes the information used in the differential diagnosis of osteitis, skull osteomyelitis and
the conditions explained above.
27
CHAPTER FOUR
MATERIALS
For this research project, I analyzed four contemporary skeletal collections from the state
of Florida, eager to identify the demographics and potential causes of skull osteomyelitis and
osteitis. I only examined skulls; therefore, only remains in which the cranium was present were
analyzed. The first collection I examined was from the Human Skeletal Donation Program under
the custody of Dr. Heather Walsh-Haney (co-investigator) located within Florida Gulf Coast
University’s Merwin Hall (Appendix A: Figure 4.1). At the time, the collection consisted of
approximately twelve (12) complete human skeletal remains, along with six (6) isolated crania,
and more than four (4) isolated maxillae and mandibles. These donated human remains were
packed in acid free boxes and stored in a laboratory room under regulated temperatures and
limited access, persevering them in excellent condition.
The second skeletal sample was located inside the evidence room within District 15
Medical Examiner’s Office. These remains are under the custody of Dr. Michael Bell; Chief of
the Medical Examiner’s Office for Palm Beach County and comprises approximately eightyseven (87) unidentified human skeletal remains. The office personnel keeps each skeleton in
separate boxes and their condition is remarkable. More than half of the skeletal remains was
available for analysis (because skulls were present) with the understanding that my analysis may
help in the resolution of the medical examiner’s cases.
I examined the second skeletal remains set under care of Dr. Heather Walsh-Haney which
were held within the specimen room of Collier County Office of the Medical Examiner. This
collection includes human remains from Jacksonville, Naples, and Panama City, Florida. I
evaluated one- hundred and forty (140) individuals; yet, eight-five (85) of these individuals were
28
absent crania; thus, excluded from analysis. I examined the remains with the understanding that
my findings may help in the resolution of these cases. Analogous to the Palm Beach County’s
storage methods, each set of remains were packed inside a box and labeled with the appropriate
case numbers.
The last collection I evaluated came from the University of Miami and curated by their
forensic anthropology lecturer Monica Faraldo, M.A. This collection is set inside the laboratory
room of the Anthropology Department and includes seven complete skeletons. In addition, there
are numerous isolated calottes, humeri, radii, ulnae, femora, tibiae and fibulae. Mrs. Faraldo
indicated that these remains belonged to University of Miami Medical Science Campus and were
previously dissected by medical students as part of a gross anatomy course.
INVENTORY
I created a new individual identification number for each skeletal remains. When present,
each cranium was examined for completeness and level of fragmentation following methods
outlined in Standards for Data Collection from Human Skeletal Remains (Buikstra and Ubelaker,
1994). If fragments were found, I re-assembled the pieces. My examination method started with
demographics (ancestry, age, and sex) followed by the antemortem pathological analysis. If
some skull bones were absent, I continued to analyze the rest and excluded the missing bones
from the examination. I recorded not applicable (NA) when bones were missing or lacked
landmarks needed for age, ancestry and sex estimation.
DEMOGRAPHICS
Statistics, although complex, are very powerful tools used to analyze current data in an
organized manner. The Center for Disease Control and Prevention (CDC) uses statistics to
29
acknowledge the amount of risks and threats a condition has caused over a period of time within
a specific place. These studies are intended to avoid epidemics and pandemics. With this in
mind, my research study was focused on determining the demographics and current statistics of
skull osteomyelitis or osteitis through the examination of human remains.
Paleodemography is known to be an important method of research for physical
anthropologists who study prehistoric populations (White, 2012). Demography is the statistical
study of current populations; specifically birth and mortality rates, population growth, size and
density of populations. The analysis of modern skeletal remains that are not from a cemetery
sample, tends to merge the theory and methods from both types of analyses to describe the
skeletal sample.
In recent times, physical anthropologists have concentrated in finding accurate methods
that will aid them in estimating skeletal age-at-death; nonetheless interobserver error, e.g.
different individuals performing the same task but obtaining different results, is still major
concern with each method (White, 2012). In addition, postmortem and taphonomic changes have
been demonstrated to cause difficulties when estimating when a fracture occurred, e.g.
antemortem, perimortem, or postmortem (Quatrehomme and Iscan, 1997).
Skeletal Age Estimation
As a best practice procedure, outlined by the Scientific Working Group for Forensic
Anthropology (SWG-ANTH), I estimated skeletal age and provided the findings within age
ranges (Adams, 2000). Since most of the individuals were isolated crania, I obtained skeletal
age-at-death primarily using the cranial vault suture fusion methods by Meindl and Lovejoy
(1985). Because cranial vault suture analysis tends to be a less reliable method, when possible I
included other age estimation techniques (Key et al, 2005). Specifically, I examined the
30
obliteration of the maxillary sutures (Mann, 1987), the sternal end of the right four (4) rib (Iscan
and Loth (1984), the auricular surface (Meindl and Lovejoy, 1985), and pubic symphysis
(Suchey-Brooks, 1990)
Sex Assessment
The estimation of biological sex is an extremely crucial step to complete when analyzing
human skeletal remains. Bones tend to be dimorphic elements, which means that while in the
process of evaluation scientists can determine if a bone belonged to a male or female. Sexual
dimorphism is most pronounced in adults than subadults (White, 2012). Generally, females are
known to be more gracile and smaller in size; whereas, males are considered more robust and
larger (Byers, 2011, White, 2012).
Multiple postcranial bones, such as the scapula, humerus, and radius have been studied
with the intent of accurately identifying sex from complete or fragmented skeletal remains. For
example, Stewart (1979) measured the diameter of the humeral head and found the distinctive
value ranges likely to be found in males and females (Byers, 2011). Similarly, the femoral head
and tibia have been intensively studied for sexing purposes and yielded strong results (Spradley,
2011). Even though metric assessment of postcranial elements are reliable sexing methods, in
this study I mainly focused upon determining sex based on the cranial features and pelvic
characteristics (Appendix B: Table 4.1). I examined cranial features following Ascadi and
Nemeskari’s (1970) scoring system for sexual dimorphism (in Buikstra and Ubelaker, 1994).
When the pelvis was available, I used the Phenice technique (1969) for sex determination, as
well as Walker’s drawings for sex differences in the greater sciatic notch and preauricular sulcus
(in Buikstra and Uberlaker, 1994).
31
Ancestry Assessment
Along with age and sex, I also estimated the ancestry of each cranium. Identifying the
ancestry group of an individual is as important as any other demographic variable, since it
provides law enforcement personnel with additional information about the decedent and perhaps
leads them to a positive identification (Byers, 2011). Moreover, ancestry determination in this
study may lead to the identification skull osteomyelitis or osteitis since the conditions tends to
predilect Europeans.
There have been different debates about which is the correct label to use when classifying
ancestry. Byers (2011) uses the terms “White” when referring to an individual of European
ancestry, “Black” for individuals of African descent, and “Asian” for the American Indians and
individuals from Asia. Nonetheless, for this project I followed Dr. Heather Walsh- Haney’s
methodology and classified individuals as European for the “Whites”, African for “Blacks”, and
Asians for the Native Americans and individuals from Asia. I completed my analysis using GillKing’s (2005) cranial morphological features (Appendix B: Table 4.2). My assessment was
completely based on my nonmetric findings of the cranial features (Appendix B: Table 4.3).
32
CHAPTER FIVE
METHODOLOGY
Biologically, the human body goes through various processes that result with skeletal
modification during life (White, 2012). For skeletal analysts, antemortem trauma and pathology
is identified by those skeletal changes associated with disease, environmental changes, or
traumatic injuries that could have marked the skeleton before death. In this study, I also
examined eight (8) additional cranial pathologies (i.e., cribra orbitalia, otitis media,
cholesteatoma, porotic hyperostosis, linear enamel hypoplasia, auditory exostoses, periodontal
disease, dental abscesses) to determine if a co-occurrence of skull osteomyelitis/osteitis and the
conditions existed and if so to what degree.
I grossly analyzed each pathological condition using a flashlight, dental mirror, and hand
lens. In some instances, I used soft brushes and dental picks to clean the bones to facilitate my
analysis. I used ABFO scales to determine the diameter of the lesions.
Skull Osteomyelitis & Osteitis
Even though skull osteomyelitis is considered a rare condition it is also an extremely
complex pathological condition difficult to diagnose due to its location and wide-ranging
symptoms (Chandler, 1986; Blyth, 2010; Ortner, 2003; Furstenberg, 1934). Skull osteomyelitis
(SO) requires clear visualization of the internal table of the skull. I recorded the location, depth,
and pattern of erosion for all of the lesions. Due to the similarities of the SO lytic lesions and PG,
I excluded from the analysis those granulations that were within the meningeal grooves and/ or
in-close proximity to the sagittal or coronal sutures. In addition, the porosity of the granulations
was an important determinant when concluding the origin of the granulation. White (2012)
describes blastic or sclerotic granulations as those lesions in which the process of bone
33
deposition has already began. On the contrary he explains that lytic or porotic lesions meant that
the infection process was still active, which would cause bone destruction. Blastic lesions would
present with smooth and regular margins, whereas lytic lesions will have thin borders. Taking
into account the previous descriptions, my analysis for presence or absence of skull
osteomyelitis/osteitis was based on the presence of deep granulations within the frontal, parietals,
and occipital bones far from the meningeal grooves or cranial sutures that appear to be blastic or
lytic (Appendix A: Figure 5.1). As for the temporal bone, I labeled them positive for skull
osteomyelitis/osteitis if there were segments of the bone destructed. With the sphenoid, unlike
the other skull bones, I determined the presence of skull osteomyelitis/osteitis if there was any
portion of the bone marked by active lytic lesions or bone remodeling (Appendix A: Figure 5.1).
The last are lesions that appear to be blastic, but if untreated it can lead to bone destruction. The
mandible was also examined for skull osteomyelitis or osteitis. Most individuals with mandibular
osteomyelitis exhibit the condition inside one or both mandibular foramens (Appendix A: Figure
5.1). There were several individuals in which skull osteomyelitis/osteitis was present in more
than one bone; in those cases I documented each of the affected bones.
Otitis Media
Similarly to skull osteomyelitis and osteitis, my method of examination for otitis media
was based on the presence or absence of lytic or blastic lesions within the temporal bone. Since
otitis media affects the inner portion of the temporal bone, its examination process was mostly
focused on the appearance of the petrous pyramid (Appendix A: Figure 5.2). I documented
“present” for those remains which exhibited lesions whether uni- or bilateral.
34
Auditory Exostoses
Bony projections found in or around the external auditory canal (EAM) visible to the
naked eye are known as auditory exostoses. For this study, I examined both the right and left
temporal bones looking for the presence of exostoses (Figure 5.2). Generally, these projections
tend to be bilateral; nonetheless my findings were based on my sense of touch and macroscopic
examination.
Cholesteatoma
Cholesteatomas manifest in dry bone as an extra opening to the temporal bone adjacent to
the EAM (Appendix A: Figure 5.3). I recorded the lesion as present or absent whether uni- or
bilateral.
Cribra Orbitalia and Porotic Hyperostosis
I examined the crania for evidence of cribra orbitalia and porotic hyperostosis using
macroscopic methods (Appendix: Figure 5.4). I used Ortner’s (2003) description to identify the
lesions. Although, he identified three stages (Stage 1: the surface is slightly porotic or fine
grained usually affecting the parietals, frontal and occipital; Stage 2: more areas of porosity
within the vault and the pitting is more irregular; Stage 3: porosity holes are clearly enlarged
forming spaces) (p.192). Irrespective of the stage of development, I recorded the lesions as
present or absent.
Linear Enamel Hypoplasia
Dental hypoplasias, also known as linear enamel hypoplasia (LEH), are transverse lines
typically found among the maxillary dentition (Appendix A: Figure 5.5). These lines are caused
35
by a disruption of the enamel formation during childhood. Although, these transverse lines are
visible during the examination process I also used a magnifying glass because, sometimes, these
lines can be vague and thin making it difficult to recognize. I recorded the lesions as present or
absent.
Periodontal Disease
Periodontal disease is a pathological condition in which teeth loosen due to alveolar bone
resorption. In most cases this condition is present even if there are little or no evidence of caries
(Ortner, 2003). An example of this condition is seen in (Appendix A: Figure 5.6). The
mandibular teeth of the first individual are all affected by periodontal disease as seen by the root
exposure. Figure 5.6 also displays the maxillary bone of another individual affected as well by
periodontal disease. In the last individual, there was such an enormous amount of bone
destruction that the only thing that could hold the teeth in place was dental wax. I scored these
lesions as present or absent.
Dental Abscess
The caries bacteria are the most common sources of tooth and maxillary and mandibular
bone infection. A dental abscess is a complication in which a collection of pus creates a cavity
that destroys the adjacent alveolar bone and exposes the tooth root apices. In my dental analysis,
I examined the condition and quality of the teeth. If there was root exposure of a specific tooth, I
did a further examination to determine if the exposure was associated with an abscess or
periodontal disease (Appendix A: Figure 5.7). I recorded these findings as present or absent.
36
CHAPTER SIX
RESULTS
I analyzed all of these data using SPSS Statistics Version 21.0 for Mac OS users. A total
of 121 crania were examined for the presence or absence of skull osteomyelitis/osteitis with the
sample comprising more males (67.6%) than females (32.4%). Even though, eighty one (81)
individuals lacked any evidence of skull osteomyelitis/osteitis, I still report the demographic
information and data from the other eight cranial pathologies.
Appendix B (Table 6.1) shows the descriptive characteristics (sex, age, ancestry) of those
individuals without skull osteomyelitis/osteitis. The minimum age for the subjects was 28–yearsold while the maximal age median was 56–years-old. The FGCU donated remains evinced an
age range of 35–56-years-old. European ancestry was the most common ancestry group with 31
individuals (44.9%) while African and Asian ancestry groups each presented with 19 (27.5%)
individuals.
There were a total of 40 (33%) individuals with skull osteomyelitis or osteitis. The
demographic data (sex, age, ancestry) of those individuals are illustrated in Appendix B (Table
6.2). Similar to the individuals without skull osteomyelitis, this group also consisted of more
males (N = 33 or 82.5%) than females (N = 7 or 17.5%). The final age range for this group was
from 33–62-years-old. My comparison of the age range from those individuals without skull
osteomyelitis/osteitis to those with the condition indicated that older individuals were more
likely to present with the condition. Nonetheless, the age range for the group with skull
osteomyelitis or osteitis is larger than for the group without the condition, which provides a
greater chance for individuals to be affected by skull osteomyelitis or osteitis. Moreover,
previous researchers had established that geriatric individuals (65+ years-old) are more likely to
37
present skull osteomyelitis/osteitis; yet, these findings showed that the condition was present on
individuals younger (< 65 years) than previously recorded (Chandler, 1986).
The ancestry groups with skull osteomyelitis/osteitis are shown in Appendices B (Table
6.2) and A (Figure 6.1). As the graph shows, in three of the collections, there were more
European individuals 22 (56.4%) than any other ancestral group. There were eight (20.5%)
individuals of Asian ancestry and nine (23.1%) individuals from African ancestry. The FGCU
skeletal remains consisted of individuals from European and Asian ancestry; whereas, all the
remains from the University of Miami were Asian. Collier County, surprisingly, presented with
the same numbers of individuals of European and Asian ancestry. Palm Beach County only
presented with one individual of Asian ancestry.
To better acknowledge and understand the prevalence of skull osteomyelitis/osteitis
between sexes and different age ranges, I conducted further analyses (Appendix B: Table 6.3). I
divided the age ranges into five different groups. When I parsed the age groupings by sex, I
found that only two (2) males and one (1) female from the younger group (≤ 29.9 years)
exhibited the condition. Ten males in the 40–49.9-year-old age grouping had skull osteomyelitis
or osteitis. The group of older individuals (50+ years) presented with 14 males and 3 females.
Overall, there were 40 individuals with skull osteomyelitis/osteitis with skeletal age being
determined for thirty seven (37) individuals.
In this study the location of the lytic lesions was important to establish because the lesion
location tends to help identify the etiology of the lesions and condition. Appendix B (Table 6.4)
shows the location of lytic lesion per individual and collection.
Out of the 40 individuals with skull osteomyelitis or osteitis, only eight (20%) affected
one bone with most lytic lesions appearing on more than one bone. Appendix A (Figure 6.2)
38
displays the frequency of lesions per skull bone. This graph illustrates that the most frequently
affected bone was the frontal (28%) followed by the temporal (23%). The parietals (20%) were
the third most common bone placing the sphenoid in the fourth position (18%). The fifth position
is occupied by the occipital (6%) and lastly the mandible (5%) with only four individuals having
the condition.
The third major part of this study was to determine the co-occurrence of skull
osteomyelitis or osteitis with cranial conditions, such as otitis media, cholesteatoma, auditory
exostoses, cribra orbitalia, porotic hyperostosis, linear enamel hypoplasia, periodontal disease,
and dental or periapical abscess. Appendix A (Figure 6.3) illustrates the percentage of cooccurrences of each condition. It is important to note that the most frequent pathology was
periodontal disease (24%) followed by otitis media (21%). The least likely to co-occur with skull
osteomyelitis/osteitis were cholesteatomas as evidenced by only one individual.
In total, there were 102 co-occurring pathologies with skull osteomyelitis/osteitis. Eight
pathologies were examined for co-occurrence (mean co-occurrence = 12.75 individuals). In order
to determine the mean number of pathologies per individual, I divided 12.75 by 40 (total number
of individuals with skull osteomyelitis/osteitis) which indicated that 0.318 (or nearly 32%) was
the probability of co-occurrence. Afterwards, I ran the One-Sample Chi-Square test to determine
if there was a difference between the expected and the observed frequencies (Appendix B:Table
6.5). The probabilities were set as 0.32 (32%) present and 0.68 (68%) absent.
As the tabulated data illustrates, the co-occurrence frequency of auditory exostoses and
porotic hyperostosis with skull osteomyelitis/osteitis was statistically insignificant with the
observed numbers of cases being close to the number of expected cases. I hypothesized that
thirteen (13) individuals with auditory exostoses would be found but only seven (7) were
39
observed. Likewise, for porotic hyperostosis I hypothesized that twelve (12) individuals would
have the condition while only eight (8) evidenced the lesions. When I compare these two
conditions with others such as otitis media (expected= 12; observed= 20) or cholesteatoma
(expected= 11; observed= 1) I realize that their significant values were due to the number of
observed individuals that either surpasses or was less than half of the individuals expected.
Even though the previous data showed that auditory exostoses and porotic hyperostosis
were not statistically significant; six (6) out of these eight (8) conditions positively or
significantly co-occurred with skull osteomyelitis/osteitis. Therefore, I concluded that otitis
media, cribra orbitalia, periodontal disease, periapical abscesses, cholesteatoma, and linear
enamel hypoplasia co-occurrence values were not equal to the mean number of pathologies per
individual.
Once I determined the degree of pathological co-occurrence, my last step involved
identifying the numbers of males and females with each condition (Appendix A: Figures 6.4 &
6.5). In general, males outnumbered females in each sample. Nevertheless, among both sexes
periodontal disease was the most common pathology. The incidence rate among males was also
higher (more than 15 individuals) for otitis media, cribra orbitalia and periapical abscesses.
Seven (7) females were diagnosed with skull osteomyelitis/osteitis with the majority of females
being afflicted by more than one condition. None of the females presented cholesteatomas,
auditory exostoses, or lineal enamel hypoplasia
40
CHAPTER SEVEN
DISCUSSION
Defining the general demographics of skull osteomyelitis or osteitis with the results from
this study is a difficult if not an impossible task. According to Wood (1992) demographic studies
based upon analysis of skeletal remains are inaccurate because researchers tend not to possess
enough information about the amount of exposure and/or risk the decedent may have
experienced during his/her lifespan or how the disease acts at the individual level. Moreover,
demographic studies need to be conducted with an unchanging, i.e. stable, population. The fact
that our skeletal sample comes from four different Florida regions with intrinsically high
migration rates impedes the creation of a definite demographical report. In addition, there’s a
need for a larger sample of female skeletal remains. Nonetheless, my comparison of the results
of this study (Table 6.2) with those previously published, i.e., skull osteomyelitis being a rare
condition where the typical patient is a geriatric male as found by researchers Chandler (1986 &
1989), Pincus (2009), Blyth (2010) and Laventhal (2011), I cannot confirm that skull
osteomyelitis is a rare pathological condition.
In my sample of 121 crania, 40 (33%) exhibited skull osteomyelitis or osteitis. My
findings showed incident rates that were higher than any other published. Moreover, the clinical
history or cause and manner of death were unknown to me. This last statement is of significance
since I was able to examine remains of individuals in which death might not have been of natural
causes and still 33% exhibited skull osteomyelitis or osteitis. Nevertheless, my findings did
support the published sex ratios with this sample evincing that the disease favors males
33(82.5%) over females 7(17.5%).
41
My findings regarding the age distribution of the pathology contradict those formerly
published. In this study, the median age range was (33–62-yearsold) with most individuals being
over 50-years-old (Table 6.3). Even though the older males presented with the condition in this
study, they were still younger than the geriatric males in previous studies. These last results were
surprising because I had expected that most of the positive individuals would be 65+years-old. I
based my expectations on previous publications (Chandler, 1986, Blyth, 2010, Pincus, 2009) and
on the idea that the samples provided by the state of Florida would be mostly geriatric and retired
individuals. Therefore, skeletal analysts, medical examiners and clinicians should consider that
individuals younger than 65- years-old may have the condition when conducting differential
diagnoses and medical treatments.
The location of the lytic lesions also yielded some unexpected results. First of all, the
most common bone to exhibit skull osteomyelitis/osteitis was the frontal bone with (25)
individuals. At first, I assumed that the lesions might be linked to another cranial condition
known as Hyperostosis Frontalis Interna (HFI); yet, this condition is more frequent in females
than in males which contradict our results. Furthermore, a frontal bone affected by HFI would
exhibit thickening and buildup of the inner table instead of the lytic lesions I observed (Ortner,
2003). As such, I concluded that the frontal lesions must be associated to osteomyelitis, osteitis
or metastatic cancer as concluded in the differential diagnosis chapter.
The temporal bone was the second most common bone exhibiting lytic lesions. Otitis
media is a condition that requires a clinical assessment of the living subject by a physician.
Nevertheless, because there is no dearth of data that links petrous pyramid lytic lesions to
osteomyelitis secondary to a bacterial infection triggered by otitis media, I interpret my data as
42
strongly supporting the clinical findings. Additional analysis, such as histological sections of
these lesions, should be performed to comprehend the etiology of the lesions.
The parietals had a total of eighteen (18) individuals exhibiting lytic lesions. At the
beginning of this study I expected that the parietals were going to be the most commonly
affected bones based on the results of my pilot study (De La Paz, 2014) and previous research
(Chandler, 1989; Ortner, 2003). The numbers of individuals with parietal lesions were not
sufficient to put these bones among the top two affected, as was the case in the pilot study.
Within the parietals, there were some discrepancies with certain individuals caused by the
location and margins of the lesions. These discrepancies were due to this study’s protocol and
resulted with exclusions which might have explained the reduced number of positive individuals.
The protocol in this study specifies that lesions too close to the sagittal and coronal sutures or
within the meningeal grooves were not going to be included due to the similarities shared with
normal PG. Therefore, there were more than two individuals whom I excluded from the study
because the margins of the lesions were not lytic or the lesions were too close to the cranial
sutures. Hence, I believe that a further analysis using radiographs and histological sections must
be conducted to clarify the depth of the lesion and the condition of the bone cells. If the lesions
are a consequence of osteomyelitis, the histological sections should demonstrate unbalanced
quantities of osteoclasts and osteoblasts.
Another interesting result achieved with this study was the number of positive sphenoid
cases. This bone occupies the fourth position in the frequency of lytic lesions. The marks within
the sphenoid were mostly found within the greater wing and on occasion I observed active
ectocranial lesions. Although, the sphenoid is a flat bone with little diploë or bone marrow, I
analyzed several individuals with active lytic lesions and bone remodeling. Due to the location of
43
the lesions I concluded that the osteomyelitis/osteitis on those individuals may have arisen from
a sinus infection that became hematogenous.
As for the occipital, I only identified five individuals with the condition. Due to the
location of the lesions, I suspected the etiology to be linked to a bacterial infection that spreads
using the venous system instead of a sinus infection that spreads due to the close proximity to the
temporal and sphenoid bones. Lastly, the mandible presented with fewer individuals (5%) than
any other bone despite the high occurrence of dental pathologies.
In the analysis of co-occurrence between skull osteomyelitis/osteitis and the different
cranial pathologies, periodontal disease was the most frequent condition to co-occur with skull
osteomyelitis/osteitis. Despite the fact that this information seems inconsistent; in my
examination process I examined the maxilla and mandible for presence or absence of the
condition. I did not specify in my notes which of the two dental arcades presented the condition.
Furthermore, not every set of remains analyzed had a complete skull. In some individuals, the
mandible was missing and precluded from the analysis. The end result was that the mandible
had the fewest cases of osteomyelitis and yet there were multiple individuals with periodontal
disease (24%) and dental abscesses (18%). These results can be explained by the incompleteness
of the skeletal remains and/ or that most individuals presented periodontal disease and dental
abscesses within the maxilla. On follow-up investigations researchers should specify the bone
and side that presents the condition in order to avoid misinterpretations.
Regarding the co-occurrence and etiology of skull osteomyelitis or osteitis, only auditory
exostoses (x2 = 0.051) and porotic hyperostosis (x2 = 0.151) presented with co-occurrence values
equal to the mean numbers of pathologies per individual. These results favor my null hypothesis,
implying that these two conditions do not co-occur with skull osteomyelitis.
44
On the other hand, cribra orbitalia does co-occur with skull osteomyelitis/osteitis (x2 =
0.006). Likewise, co-occurrence values were significant with regard to periodontal disease (x2 =
0.000), cholesteatomas (x2 = 0.000), otitis media (x2 = 0.006), periapical abscesses (x2 = 0.017)
and linear enamel hypoplasia (x2 = 0.02). Each of the previous conditions begin as bacterial
infections at a specific site (teeth, auditory canal, or frontal bone) with possibilities of becoming
hematogenous infections that spread using the facial sinuses or venous system. This finding also
suggests that the etiology of cribra orbitalia and porotic hyperostosis may not be connected
(Ortner, 2003; Walker, 2009).
The etiology of skull osteomyelitis and osteitis is complicated and probably
multifactorial. Osteomyelitis is defined as a nonspecific bone infection. Based on the test for cooccurrence, this condition most likely develops secondary to a bacterial infection caused by
periodontal disease or otitis media. Yet, if I focus my results on the bones most commonly
affected by skull osteomyelitis or osteitis I would conclude that this disease began as an infection
that spreads and progresses through the sinuses affecting the frontal, sphenoid, and parietals.
The results of this study confirmed that there are numerous amounts of conditions which
may incite osteomyelitis. If new scientific research is conducted on this condition, the clinical
history of the subject, comparison of in-life and after death radiographs, and histological sections
of the lesions should be added to the data that is collected. If histology studies are not possible,
the researcher should consider using a dissecting microscope to better acknowledge the margins
and porosity of the lesions. This instrument would provide better lighting that facilitates the bone
examination process. Moreover, the examination of the postcranial skeleton would also aid in
determining the presence or absence of other systemic infections somewhere else in the skeleton.
45
In respect to this investigation, I prefer to classify the condition under this study as
osteitis instead of skull osteomyelitis. Even though my analysis and protocol was completely
based on the assumption that this condition was skull osteomyelitis, the fact that there were no
cloaca in the crania and that I could not determine if the lesions were a result of an infection
within the bone marrow or an infection that affects the bone thickness, leads me to consider that
these individuals might have presented with infections of the compact bone of the inner table
instead of the bone marrow. Metastatic cancer is still a plausible diagnosis, but the lack of lesions
in the outer table makes me conclude that osteitis is a more accurate diagnosis.
To conclude, I would like to highlight the remains from Collier County. One individual
presented lytic lesions within the frontal bone, coronal suture, and sphenoid (Appendix A: Figure
7.1). At first, I doubted the possibility of including this individual as part of the positive cases
with skull osteomyelitis/osteitis, since the majority of the lesions are found within the coronal
suture. However, additional lytic lesions were found proximal to the frontal sinus and among the
greater wing of the sphenoid. For that reason, I added the case information to the skull
osteomyelitis/osteitis data.
Of particular interest is that my study protocol excludes cases with lytic lesions located
within the meningeal grooves, coronal or sagittal sutures. The fact that I was able to observe
additional lesions among the frontal and sphenoid bone allowed me to add this diseased
individual to our sample. These remains are of remarkable importance since they are a clear
representation of an endocranial hematogenous infection. In addition, this individual exemplifies
the necessity of a new study and protocol that examines each lytic lesion within the skull
regardless of their location or depth. The subject’s clinical history with the addition of
radiograph and a histological assessment would prove invaluable for future studies.
46
CONCLUSION
The study of human skeletal remains provides researchers and physicians with insights on
the manifestation and severity of diseases. This study analyzed lytic lesions from four modern
Floridian samples in an attempt to identify skull osteomyelitis or osteitis. Forty individuals
within this sample exhibited endocranial lytic lesions. Based on the lesion appearances and
location within the crania I concluded that the condition under study was osteitis instead of skull
osteomyelitis. I make this determination based upon the fact that there were no cloaca in the
crania and that I could not determine if the lesions were a result of an infection within the bone
marrow or an infection that affects the thickness of the bones. Furthermore, this study show that
osteitis most frequently co-occurs with periodontal disease and in decreasing order of frequency
otitis media, cribra orbitalia, dental abscesses, linear enamel hypoplasia, and cholesteatomas.
Osteitis did not significantly co-occur with auditory exostoses or porotic hyperostosis. The fact
that more than one condition co-occurs with osteitis suggests that this condition is non-specific
and can develop under multiple circumstances and/or locations.
As a final thought, this study confirms that endocranial lytic lesions are more likely to
develop in older males than in females. The sample and results obtained from this study are of
significant importance since it is composed of individuals from both biological sexes, different
age ranges and ancestry groups, and whose death was not necessarily the result of a pre-existing
medical condition that resulted in death. Furthermore, my analysis may help in the resolution of
the medical examiner’s cases and also aid physicians with the new data for differential diagnosis,
cause and manner of death, as well as, assessment of overall community health.
47
APPENDIX A
Figure 3.1.: Data flow diagram of possible differential diagnoses.
48
Figure 4.1: Overall photograph of the Human Donation Laboratory at Florida Gulf Coast University,
April 2014.
49
Figure 5.1: Macroscopic photographs of the frontal bone (top left) and right parietal (top right) showing lytic foci;
greater wing of the right sphenoid with lytic foci and active bone remodeling (middle); right mandibular foramen
with lytic lesions.
50
Figure 5.2: Macroscopic photographs of the petrous portion of the left temporal bone presenting bone destruction
(left); bony projection on the left external auditory canal (right).
Figure 5.3: Macroscopic photographs of a Foramen of Huschke (red oval) and Cholesteatoma (blue arrow); lytic
lesions within the middle portion of the temporal bone.
51
Figure 5.4: Macroscopic photographs of the right frontal bone with cribra orbitalia (left) and parietal bones with
porotic hyperostosis (right).
Figure 5.5: Macroscopic photograph of the maxillary dentition with evidence of linear enamel hypoplasia (red arrow).
52
Figure 5.6: Macroscopic photographs of an individual's mandible affected by periodontal disease, right lateral view
(top left), left lateral view (top right), anterior view (bottom left); left maxilla with evidence of alveolar bone
destruction (bottom right).
53
Figure 5.7: Macroscopic photograph of the left maxillary dentition with evidence of multiple dental abscesses.
54
UM
DP
Asian
African
European
C
PB
0
1
2
3
4
5
6
7
8
9
10
Figure 6.1: The Frequency of Ancestry Groups on Individuals with Skull Osteomyelitis/Osteitis by Collection.
Legend: UM- University of Miami, DP- FGCU Donation Program, C- Collier County MEO and WP- Palm Beach County MEO
55
30
25
Incidence
20
15
10
5
0
Frontal
Sphenoid
Parietals
Temporal
Occipital
Mandible
Bone
Figure 6.2: The Frequency of Individuals with Skull Lytic Lesions from Four Floridian Skeletal Collections by Bone.
56
Linear Enamel Hypoplasia
3%
Cholesteatoma
1%
Hipertosis Cranii
8%
Otitis Media
21%
Periapical Abcess
18%
Cribra Orbitalia
19%
Auditory
Exostoses
6%
Periodontal Disease
24%
Figure 6.3: The Frequency of Co-Occurrence of Skull Osteomyelitis/Osteitis by Pathology from four Floridian Skeletal Samples.
57
20
18
16
14
Incidence
12
UM
10
DP
C
8
WP
6
4
2
0
OM
CO
PD
AE
PA
Pathologies
CH
HC
LEH
Figure 6.4: Incidence of Pathologies among Males with Skull Osteomyelitis/Osteitis by Sample.
Legend: UM- University of Miami, DP- FGCU Donation Program, C- Collier County MEO, WP- Palm Beach County MEO, OM- Otitis
Media, CO- Cribra Orbitalia, PD- Periodontal Disease, AE- Auditory Exostoses, PA- Periapical Abscess, CH- Cholesteatoma, HC- Porotic
Hyperostosis and LEH- Linear Enamel Hypoplasia.
58
6
5
Incidence
4
UM
3
DP
C
WP
2
1
0
OM
CO
PD
AE
PA
Pathologies
CH
HC
LEH
Figure 6.5: Incidence of Pathologies among Females with Skull Osteomyelitis/Osteitis by Sample.
Legend: UM- University of Miami, DP- FGCU Donation Program, C- Collier County MEO, WP- Palm Beach County MEO, OM- Otitis
Media, CO- Cribra Orbitalia, PD- Periodontal Disease, AE- Auditory Exostoses, PA- Periapical Abscess, CH- Cholesteatoma, HC-Porotic
Hyperostosis and LEH- Linear Enamel Hypoplasia.
59
Figure 7.1: Macroscopic picture of the inner table exhibiting lytic lesions along the frontal bone and coronal suture
60
APPENDIX B
Table 4.1- MALE AND FEMALE SEXING CHARACTERISTICS
FOR THE SKULL AND PELVIS
Skull
Pelvis
Female
Small in size, smooth glabellar and
nuchal areas, sharp supraorbital
margin, non-projecting nuchal area,
and pointed chin.
Small and gracile, low ilium, broad
subpubic angle, patent ventral arc,
triangular obturator foramen, wide
greater sciatic notch (GSN), and short
sacrum.
Male
Large in size and robust, large glabellar
region, rounded supraorbital margin, rugged
nuchal area with an inion hood, and broad
mental eminence.
Large and robust, high ilium, narrow pubic
shape, large obturator foramen, narrow
(GSN), lack of preauricular sulcus and ventral
arc, and a long and narrow sacrum.
After Krogman (1962) in Byers (2011).
Table 4.2- CRANIAL MORPHOLOGICAL FEAUTURES FROM THE
THREE MAJOR ANCESTRY GROUPS
African
Post-bregmatic depression
Simple cranial sutures
Rectangular Orbits
S-shape zygomatico-maxillary
suture
Long base chord
Nasal guttering
Small nasal spines
Crenulated molars
Prognathism
Hyperbolic dental arcade
Rounded EAM
Bulging palatine suture
Small nasal spines
Native American & Asian
Complex cranial sutures
Short base chord
Round orbits
Angled zygomatico-maxillary
suture
Intermediate nasal spines
Wormian bones
Projecting zygomatics
Malar tubercule
Elliptical dental arcade
Straight palatine suture
Shovel shaped incisors
Wide interorbital breadth
Straight palatine suture
European
Simple cranial sutures
Angle orbits
S-shape zygomatico-maxillary
suture
Bulging palatine suture
Inion hook
Metopic trace
Depressed nasion
Long base chord
Long nasal spines
Nasal sill
Carabelli’s cusps
Narrow interorbital breadth
Bulging palatine suture
Adapted from George W. Gill (2005)
61
Table 4.3: DESCRIPTIVE CHARACTERISTICS OF FOUR FLORIDIAN SKELETAL SAMPLES
Collection
Characteristics
Sex
Male
Female
Age minimum
Age maximum
Median
Mean
St. Deviation
Median
Mean
St. Deviation
Ancestry
African
Asian
European
Total
n=253
Palm Beach County
(n=86)
Collier County
(n=140)
FGCU Donation
Program (n=18)
University of
Miami (n=9)
n=119
86 (72.3%)
33 (27.7%)
n=110
28
33.09
12.95
62
56.49
12.23
n=112
29 (25.9%)
30 (26.8%)
53 (47.3%)
n=41
27 (65.9%)
14 (34.1%)
n=38
28
29.45
6.69
59
56.13
10.57
n=38
12 (31.6%)
4 (10.5%)
22 (57.9%)
n=53
39 (73.6%)
14 (26.4%)
n=48
28
31.02
8.73
60
56.52
9.87
n=49
15 (30.6%)
16 (32.7%)
18 (36.7%)
n=18
15 (83.3%)
3 (16.7%)
n=17
35
47.18
22.86
62
58.24
20.41
n=18
2 (11.1%)
3 (16.7%)
13 (72.2%)
n=7
5 (71.4%)
2 (28.6%)
n=7
30
32.86
9.94
46
54
11.76
n=7
0%
7 (100%)
0%
62
Table 6.1: DESCRIPTIVE CHARACTERISTICS OF FOUR FLORIDIAN SKELETAL SAMPLES
WITHOUT SKULL OSTEOMYELITIS/OSTEITIS
Collection
Characteristics
Sex
Male
Female
Age minimum
Age maximum
Median
Mean
St. Deviation
Median
Mean
St. Deviation
Ancestry
African
Asian
European
Total
(n=81)
Palm Beach County
(n=27)
Collier County
(n=39)
FGCU Donation
Program (n=8)
University of
Miami (n=7)
n=74
50 (67.6%)
24 (32.4%)
n=71
28
30.72
8.87
59
54.65
11.12
n=69
19 (27.5%)
19 (27.5%)
31 (44.9%)
n=25
16 (64%)
9 (36%)
n= 23
28
29.35
6.24
56
56.17
8.64
n=24
7 (29.2%)
3 (12.5%)
14 (58.3%)
n=35
23 (65.7%)
12 (34.3%)
n=35
28
29.89
8.46
56
55
10.17
n=31
10 (32.3%)
8 (25.8%)
13 (41.9%)
n=8
7 (87.5%)
1 (12.5%)
n=7
35
38.57
14.02
56
49.71
20.46
n=8
2 (25%)
2 (25%)
4 (50%)
n=6
4 (66.7%)
2 (33.3%)
n=6
25
31.67
10.39
45
52.5
12.13
n=6
0%
6 (100%)
0%
63
Table 6.2: DESCRIPTIVE CHARACTERISTICS OF FOUR FLORIDIAN SKELETAL SAMPLES
WITH SKULL OSTEOMYELITIS/OSTEITIS
Collection
Characteristics
Sex
Male
Female
Age minimum
Age maximum
Median
Mean
St. Deviation
Median
Mean
St. Deviation
Ancestry
African
Asian
European
Total
(n=40)
Palm Beach County
(n=15)
Collier County
(n=14)
FGCU Donation
Program (n=10)
University of
Miami (n=1)
n=40
33 (82.5%)
7 (17.5%)
n=37
33
38
17.64
62
64.46
13.2
n=39
9 (23.1%)
8 (20.5%)
22 (56.4%)
n=15
11 (73.3%)
4 (26.7%)
n= 14
27
30.34
7.09
59
57.64
12.31
n=14
5 (35.7%)
1 (7.1%)
8 (57.1%)
n=14
13 (92.9%)
1 (7.1%)
n=12
30
34
9.45
54
60.42
8.28
n=14
4 (28.6%)
5 (35.7%)
5 (35.7%)
n=10
8 (80%)
2 (20%)
n=10
33
53.2
26.46
56
64.2
19.12
n=10
0%
1 (10%)
9 (90%)
n=1
1 (100%)
0%
n=1
40
63
n=1
0%
1 (100%)
0%
64
Table 6.3: SEX AND AGE RANGES OF FOUR FLORIDIAN
SKELETAL SAMPLES
Age Range
SO- Present
SO- Absent
Males
Females
Males
Females
under- 29.9
2
1
5
3
30-39.9
4
0
10
3
40-49.9
10
3
19
9
50- older
14
3
14
3
Total
30
7
48
18
Legend: SO- Skull Osteomyelitis
65
Table 6.4: LOCATION OF ACTIVE CRANIAL LYTIC LESIONS (ACLL)
PER INDIVIDUAL BY SAMPLE
Accession #
LL- Location
Accession #
LL- Location
WP2
WP4
WP14
WP15
WP18
WP19
WP25
WP52
WP67
Sph +Temp
Par
Par +Temp
Par +Temp
Fr + Temp
Fr + Par +Temp
Fr + Temp
Man
Fr + Par +Sph +
Temp
Fr + Par +Sph
Fr + Sph
C53
C58
C64
C72
C73
C74
C106
C112
DP-1
Fr + Par +Sph
Sph +Temp
Sph
Fr + Temp
Man
Fr
Sph
Fr + Par +Sph
Fr + Par
DP-2
DP-3
Fr +Par + Occ
Fr + Occ
Fr + Man
Fr + Par +Sph +
Temp
Man + Temp
Sph
Fr + Sph +Temp
Sph
Fr + Par +Sph +
Temp
Fr + Par +Sph
+Temp
DP-4
DP-5
DP-6
DP-7
Fr + Par + Temp
Fr +Par + Occ +
Temp
Fr + Par + Temp
Fr +Par + Occ
Par + Temp
Occ + Temp
DP-12
DP-13
DP-15
UM6
Fr
Fr
Fr + Temp
Fr + Sph
Total ACLL =
40
WP70
WP71
WP73
WP77
WP78
WP79
C1
C2
C19
C20
C21
C35
Legend: LL- Lytic lesion, WP- Palm Beach County, C- Collier County, DP- FGCU
Donation Program, UM- University of Miami, Fr- Frontal, Sph- Sphenoid, Par- Parietals,
Temp- Temporal, Man- Mandible and Occ- Occipital.
66
Table 6.5: CO-OCURRENCE OF EIGHT SKELETAL PATHOLOGIES
WITH SKULL OSTEOMYELITIS/OSTEITIS
Otitis Media
Cribra Orbitalia
Periodontal Disease
Auditory Exostoses
Periapical Abscess
Cholesteatoma
Porotic Hyperostosis
Linear Enamel
Hypoplasia
x2
n
%
df
7.518
7.518
20.03
3.818
5.731
15.45
2.058
5.371
38
38
36
40
38
39
38
27
21
19
24
6
18
1
8
3
1
1
1
1
1
1
1
1
2-sided asymptotic
significance
0.006
0.006
0.000
0.051
0.017
0.000
0.151
0.02
One Sample Chi- Square (2- sided) asymptotic significance with degrees of freedom.
67
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