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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 1 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 2 CONCLUSION…………………………………………………………………………………47 APPENDIX A……………………………………………………………………………….48–60 APPENDIX B……………………………………………………………………………….61–67 REFERENCES……………………………………………………………………………...68–73 3 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. 4 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 5 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). 6 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. 7 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, 8 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 9 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 10 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 11 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). 12 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 13 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. 14 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 15 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. 16 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- 17 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. 18 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 19 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). 20 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 21 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 REFERENCES Adams, D.E., Lothridge, K.L. 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