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Metabolic disease can be described as the body's response to physiological, and in some cases emotional, stress. It can be caused by dietary deficiencies or excesses, chronic disease, trauma, blood loss, poor hygiene, lack of medical care and deprived living conditions. Physiological stress, food intake and disease are all closely interrelated, often affecting one another. Consequently, individuals suffering from dietary deficiencies are more susceptible to infectious disease as well as stress symptoms, and in return, physical stress predisposes a person to infectious disease. Furthermore, individuals suffering from infectious diseases are likely to have a lower food intake as a result of appetite loss, which promotes the downward spiral.
The body's response to physiological stress depends on the individual's immune system, genetic predisposition and the type of stress suffered (Roberts and Manchester 1995, 164). Osteologically identifiable skeletal manifestations of long-standing metabolic conditions include increases or decreases in bone resorption (osteoporosis, cribra orbitalia or formation (scurvy) among others (Brickley 2000, 184).
Iron deficiency anaemia is one of the most common metabolic conditions, in both historic and modern populations. In Europe, the skeletal expressions (porotic hyperostosis) tend to develop in the eye orbits and are characterised by porosity cribra orbitalia, which can vary in severity (Plate 3, right). In the United States, however, the porotic lesions are more commonly seen on the outer (ectocranial) surface of the skull cribra cranii. These have also occasionally been observed in archaeological populations in Great Britain. In modern studies, between 50 and 75% of patients with iron deficiency anaemia have skeletal lesions which can be radiologically detected (Stuart-Macadam 1991, 105), implying that calculations based on the quantity of lesions provide an underestimation of the number of individuals suffering from anaemia. Furthermore, the skeletal lesions caused by iron deficiency can be indicative of periods of iron deficiency during childhood, and often remodel during late childhood or early adulthood, thus producing an even lower prevalence rate. However, these lesions can also be observed frequently in adults, and the mechanisms determining remodelling are not yet fully understood.
The causes of iron deficiency anaemia are complex, as factors affecting the development of anaemia include cultural customs, environment, climate, topography, geography, hygiene, food resources, aggregation and medical care (Stuart-Macadam 1992, 160). All of these factors can affect the pathogen load in a population, which is the most important cause of iron deficiency ibid. Bacteria tend to thrive in environments with warm climates, poor hygiene, and greater population density, causing an increased pathogen load, a rise in the rate of infection, and often widespread chronic disease. This process simultaneously stimulates the defence systems into maintaining a lowered iron status, so that the blood is a less suitable medium for bacterial development, with the aim of warding off further bouts of disease ibid, 164). The body therefore attempts to maintain a balance between its need for iron, especially in menstruating women and children whose rapid growth means that they have a greater need for iron, and the lower iron status needed to defend against pathogens ibid, 159).
In single individuals, other causes of iron deficiency include severe blood loss following injury and destruction of red blood cells (Kent 1992, 2), cancer and parasitic gut infection (Roberts and Manchester 1995, 166). Symptoms of iron deficiency anaemia include gastrointestinal disturbance, shortness of breath, fatigue, pallor and palpitations (Roberts and Manchester 1995, 167).
At Fishergate House, the prevalence of the skeletal manifestation cribra orbitalia was recorded by noting presence or absence of the eye orbit, along with the presence or absence and the severity of lesions. This was based on a system developed by Stuart-Macadam (1991, 109) which defines the affected area of the orbit and the severity of the lesion (from one to five, increasing in severity). As a result, the prevalence of lesions could be calculated.
It was found that 20% of the total population had cribra orbitalia lesions in one or both eye orbits. No lesions were observed in the foetal, neonatal and infant remains, nor in the adults of undetermined sex. The lack of lesions in the latter group was probably due to their poor preservation and incompleteness, rather than a true lack of cribra orbitalia. The greatest prevalence of iron deficiency anaemia was found in the adolescents, 47% of whom had the condition, with lesions in 75% of their orbits (Table 21). The prevalence in the juveniles was slightly lower, with only 33% of juveniles displaying cribra orbitalia (59% of the right orbits and 65% of the left orbits affected). The prevalence of cribra orbitalia in children from Fishergate House (29%) was similar to that of Hull Magistrate's Court (27.5%).
| Sex | Age group | No. of individuals | % of age group | No. of right orbits | % | Area* | Stage* | No. of left orbits | % | Area* | Stage* |
|---|---|---|---|---|---|---|---|---|---|---|---|
| U | Foetus | 0/5 | 0 | - | - | - | - | - | - | - | - |
| Neonate | 0/4 | 0 | - | - | - | - | 0/1 | 0 | - | - | |
| Infant | 0/9 | 0 | 0/4 | 0 | - | - | 0/3 | 0 | - | - | |
| Juvenile | 26/80 | 33 | 20/34 | 59 | 8 area 2 | 1 stage 1 | 22/34 | 65 | 8 area 2 | 1 stage 1 | |
| 4 area 3 | 15 stage 2 | 4 area 3 | 15 stage 2 | ||||||||
| 1 area 4 | 3 stage 3 | 1 area 4 | 6 stage 3 | ||||||||
| 10 area 5 | 1 stage 5 | 10 area 5 | |||||||||
| Adolescent | 7/15 | 47 | 6/8 | 75 | 1 area 3 | 1 stage 1 | 6/8 | 75 | 1 area 3 | 1 stage 1 | |
| 1 area 4 | 4 stage 3 | 1 area 4 | 4 stage 3 | ||||||||
| 4 area 5 | 1 stage 4 | 4 area 5 | 1 stage 4 | ||||||||
| Total | 33/113 | 29 | 26/46 | 57 | 8 area 2 | 2 stage 1 | 28/46 | 61 | 8 area 2 | 2 stage 1 | |
| 5 area 3 | 15 stage 2 | 5 area 3 | 15 stage 2 | ||||||||
| 2 area 4 | 7 stage 3 | 2 area 4 | 10 stage 3 | ||||||||
| 14 area 5 | 1 stage 4 | 14 area 5 | 1 stage 4 | ||||||||
| 1 stage 5 | |||||||||||
| F | 18-25 | 1/5 | 20 | 1/24 | 4 | 1 area 5 | 1 stage 2 | 1/24 | 4 | 1 area 5 | 1 stage2 |
| 26-35 | 1/10 | 10 | 1/24 | 4 | 1 area 5 | 1 stage 2 | 1/24 | 4 | 1 area 5 | 1 stage 2 | |
| 46+ | 5/23 | 22 | 5/24 | 17 | 1 area 2 | 2 stage 1 | 5/24 | 21 | 1 area 2 | 3 stage 1 | |
| 2 area 4 | 2 stage 2 | 2 area 4 | 2 stage 2 | ||||||||
| 1 area 7 | 1 area 5 | ||||||||||
| 1 area 7 | |||||||||||
| Total | 6/53 | 11 | 7/24 | 25 | 2 area 4 | 2 stage 1 | 7/24 | 29 | 1 area 2 | 3 stage 1 | |
| 2 area 5 | 4 stage 2 | 2 area 4 | 4 stage 2 | ||||||||
| 1 area 7 | 3 area 5 | ||||||||||
| 1 area 7 | |||||||||||
| M | 18-25 | 2/7 | 29 | 2/27 | 4 | 1 area 4 | 1 stage 2 | 2/27 | 7 | 1 area 4 | 1 stage 2 |
| 1 area 5 | 1 stage3 | ||||||||||
| 26-35 | 1/14 | 7 | 0/27 | 0 | - | - | 1/27 | 4 | 1 area 4 | 1 stage 2 | |
| 26-35 | 2/14 | 14 | 1/27 | 4 | 1 area 4 | 1 stage 2 | 1/27 | 4 | 1 area 4 | 1 stage 2 | |
| 46+ | 3/16 | 19 | 2/27 | 7 | 2 area 5 | 2 stage 2 | 2/27 | 7 | 1 area 4 | 1 stage 1 | |
| Total | 8/57 | 14 | 4/27 | 15 | 2 area 4 | 4 stage 2 | 6/27 | 22 | 1 area 2 | 2 stage 1 | |
| 2 area 4 | 2 area 4 | 3 stage 2 | |||||||||
| 3 area 5 | 1 stage 3 | ||||||||||
| All | All | 49/244 | 20 | 36/97 | 37 | - | - | 41/97 | 42 | - | - |
The severity of cribra orbitalialesions increased with age from juveniles to adolescents, but decreased in young adults, thereafter remaining constant (Figure 12). This decrease in the severity of cribra orbitalia during early adulthood is probably the result of remodelling of the lesions. The consistency of prevalence rates in adults from Fishergate House suggests that those lesions which are not subject to remodelling during early adulthood were not likely to remodel with increasing age. The persistence of the lesions in adult skeletons suggests that iron deficiency continued into adulthood - otherwise the lesions would have remodelled. Eleven percent of female and 14% of male adults suffered from cribra orbitalia, with the greatest prevalence in the young adult and mature adult groups (Table 21).
Figure 12
It is interesting to note that the prevalence of cribra orbitalia varied between the sexes and age groups at Fishergate House (Figure 13). The difference between male and female prevalence rates was small in the young adults and young middle adults, but increased in the old middle adults (Table 21) and was considerable in the mature adults, with older females exhibiting a much higher rate than males. Considering the greater likelihood of blood loss in females, the observation of a higher prevalence rate of cribra orbitalia in this group was not unexpected. This has also been commonly noted in other medieval cemeteries.
Figure 13
The severity of cribra orbitalia in other populations, such as the Romano-British group from Poundbury, Dorset, tended to show a peak in cribra orbitalia prevalence in the six month to four year age group (Stuart-Macadam 1991, 105), which was attributed to a lowered immune system during weaning. When age was divided into two-year intervals at Fishergate House, it was found that the highest prevalence rate could be observed in the eight to ten year old juveniles (56%), followed by the fourteen to sixteen year old adolescents (50%) and the birth to two year age group (47%). It is significant that the individuals with cribra orbitalia from this latter age group were all over the age of one year, suggesting that anaemia in the youngest individuals was indeed caused by weaning.
The children's prevalence of orbits with cribra orbitalia in the Fishergate House population (59% of orbits affected) was higher than the rates observed by Lewis (2002a, 55) at Raunds Furnells (55%), Wharram Percy (56%), and St Helen's-in-the-Walls, but lower than that at St Andrew's (64%). At Fishergate House, cribra orbitalia affected a lower number of the children's population (14%) than at Hull Magistrate's Court (17%) (Holst et al forthcoming), but more males (11%) and females (14%) than at Hull (8% and 12%), suggesting that the lesions were less likely to have remodelled.
The prevalence of cribra orbitalia (20%) is similar in a number of medieval populations, including Towton (23%) (Coughlan and Holst 2000), Blackfriars 19.2% (Wiggins et al 1993) and the Period 6 population from St Andrew's (21%) (Stroud and Kemp 1993). The rate was slightly higher at Hull Magistrate's Court (27.5%) (Holst et al forthcoming) and slightly lower at Jewbury and St Nicholas Shambles (15.4% and 12.4%) (Lilley et al 1994 and White 1988). These rates suggest a fairly consistent incidence of iron deficiency anaemia across medieval populations.
Six individuals with cribra orbitalia (2.4% of the population, 12% of those with cribra orbitalia also showed evidence for porosity on the outer skull table, particularly the frontal and parietals. These lesions may also have been anaemia-related; however, nine further individuals with similar porotic lesions had no evidence for cribra orbitalia in the eye orbits. It is possible, therefore, that some individuals developed only the cranial lesions following iron deficiency, or alternatively, that the cranial porosity had a different cause.
Sixty-five percent of individuals with cribra orbitalia lesions were found to have additional pathological conditions other than congenital anomalies, the majority of which were inflammatory lesions of the lower limb bones or crania (24%). Four individuals had Harris lines (indicative of arrested growth due to stress), as well as cribra orbitalia. Other conditions associated with cribra orbitalia included hydrocephalus in one juvenile, possible tuberculosis in an adolescent and a male adult, and possible rickets in three juveniles. Although iron deficiency anaemia cannot be directly associated with the pathological conditions observed, it is noteworthy that such a large part of the population who suffered from anaemia also showed evidence for other diseases, many of which were infectious. At a medieval leprosarium at Næstved, Denmark, where two thirds of the population had cribra orbitalia, a particularly high prevalence of iron deficiency anaemia was observed, which was attributed to the high pathogen load in this population caused by leprosy (Roberts and Manchester 1995, 166).
There was a generally even distribution of cribra orbitaliaacross the cemetery, although a concentration of individuals with cribra orbitalia was noted on the western edge of Intervention 1.
Harris lines are thin transverse layers of bone which form in the long bone medullary cavity that contains bone marrow. The lines develop during childhood in those cases where nutritional deficiencies, acute and chronic disease, or even emotional stress cause arrested growth of the long bones (Mays 1995, 511). However, the causes of Harris lines are complex, and in modern trials, Harris lines have been detected in children with known medical histories, despite a lack of disease or malnutrition ibid. The lines are only formed during recovery stages, when growth resumes. Harris lines may remodel during childhood and adulthood, or can persist into adulthood.
It is clear from the palaeopathological evidence that Harris lines can be attributed to a number of factors, many of which may not be visible in the skeletal remains, either because they were acute, because they affected the soft tissue rather than the bone, or because they were not of a physiological nature. However, a number of possible stress-inducing conditions were identified in the skeletons from Fishergate House, which could have led to arrested growth and the formation of Harris lines. Identification of Harris lines relied upon the visual examination of broken long bone shafts, and therefore, only a small percentage of Harris lines was actually identified.
Harris lines were observed in ten individuals (4% of the population), six of whom were juveniles under the age of six (Table 22); the remaining individuals included a young adult female, two old middle adult males and a mature adult male. The most commonly affected bone was the femur, followed by the humerus, radius and tibia; however, this may not reflect the true distribution of lesions. Research has shown that Harris lines are most common in femora, tibiae and radii, with the greatest frequency in left tibiae (Lewis 2000a, 47).
| Context No. | Age | Sex | Site of Harris line | Infection | Non-specific Infection | Metabolic condition | Healed fracture |
|---|---|---|---|---|---|---|---|
| 1071 | 1.5-2.5 | n | femur | - | - | - | - |
| 1081 | 26-35 | m | femur, tibia | - | periostitis of lower limb | - | radius, ulna |
| 1106 | 10-12 | n | tibia | - | - | cribra orbitalia | - |
| 1117 | 26-35 | m | radius | - | periostitis, osteitis of lower limb, sinusitis | rickets? | tarsals, metatarsals, fibula |
| 1163 | 46+ | m | femur | tuberculosis | periostitis, lower limb, metatarsals, ribs, osteitis of tibia, sinusitis | - | three rib fractures |
| 1165 | 18-25 | f | femur | - | periostitis of lower limb, sinusitis | cribra orbitalia | - |
| 1289 | 1-2 | n | femur | - | periostitis of jaws | cribra orbitalia, rickets? | - |
| 1333 | 1.5-2.5 | n | femur, humerus | - | - | - | - |
| 1336 | 4.5-6 | n | femur | - | - | - | - |
| 1425 | 1-2 | n | femur, humerus | - | - | cribra orbitalia | - |
Of the ten individuals with Harris lines, three showed no further evidence for pathological conditions (Table 22). However, three skeletons also had irregularities indicative of chronic sinusitis (C1117, C1163 and C1165). Five individuals suffered from non-specific infection (periosteal inflammatory lesions), which was active at the time of death in three cases (C1117, C1163 and C1289) and severe bone infection (osteitis) in two individuals (C1117 and C1163). In all but two skeletons with Harris lines and periostitis, the non-specific infection only affected the lower limbs. However, in a one to two year old juvenile C1289, the maxilla and mandible were subject to active woven bone formation, and bowing of the legs suggested that this juvenile may have suffered from rickets - this may have been a contributing factor in the formation of Harris lines. An old middle adult C1117 may also have suffered from rickets. Almost all of the right ribs, as well as both legs, were affected by active woven bone formation, indicative of tuberculosis in skeleton C1163, a mature adult male. Both rickets and tuberculosis could have caused arrested growth and the subsequent formation of Harris lines.
It is possible that chronic infection during childhood may have been the cause for the development of Harris lines in some of these individuals. However, three individuals with evidence for inflammation (C1081, C1117 and C1163) were older adults with relatively recent infections, suggesting that the Harris lines might be attributed to different causes.
Four individuals with Harris lines also had cribra orbitalia (C1106, C1165, C1289 and C1425), all but one of whom were juveniles. Both iron deficiency anaemia and Harris lines may be attributed to the same physiological stress in these individuals.
The particularly tall stature of the three males with Harris lines indicates that arrested growth during childhood did not affect their final adult height. Skeleton C1117, who had suffered from the greatest number of pathological conditions, was the third tallest person in this population. This suggests that catch-up growth occurred in the years following the stressful episode. It is therefore unexpected to find that the Harris lines did not remodel. Nevertheless, the only female with Harris lines (C1165) was the shortest individual by far in the whole population. Her short stature may be attributed to a lack of catch-up growth, possibly resulting from continuing stress, or may have been caused by another condition. However, Lewis (2002a) found that Harris lines had no affect on the growth of children in three medieval populations she studied, implying that the short stature of female C1165 may not have been related to Harris lines.
Without radiography on the long bones, it is not possible to calculate the prevalence rates of Harris Lines for this population. However, identical standards and techniques for the identification of the bony layer were used to examine broken bones at Hull Magistrate's Court. While at Fishergate House 4% of individuals were found to have Harris lines, only 0.5% of individuals had the lesion at Hull Magistrate's Court.
Rickets is caused by prolonged vitamin D deficiency during childhood, and is characterised by bowing of the weight-bearing bones. The majority of vitamin D is obtained directly from ultraviolet light. Rickets was little known before the demographic shift into cities during the post-medieval period (Aufderheide and Rodríguez-Martín 1998, 305). Industrial pollution, crowded housing, increased population density, dress customs, and children working in factories or mines during daylight hours caused a dramatic rise in rickets in the 17th and 18th centuries (Roberts and Manchester 1995, 174). Rickets became so common in British industrial centres and mining areas that it was known as the 'English Disease'. While rickets gradually increased in urban areas during the medieval period, it remained almost absent from villages (Stuart-Macadam 1989, 210-212).
Rickets tends to occur most commonly during rapid growth spurts between the ages of six months and four years, as well as in puberty, and is most prevalent in winter, when people spend less time outside (Ortner and Putschar 1985, 274; Stuart-Macadam 1989, 202). Rickets may also be seen in sick children who are kept indoors to recover from another disease. Although most archaeological cases of rickets date to the industrial period, a number of earlier examples, including prehistoric cases, have been noted (Aufderheide and Rodríguez-Martín 1998, 309).
The lack of vitamin D causes softening of the bones and cessation in cartilage mineralisation. Subsequent skeletal manifestations include bowing of weight-bearing long bones, distortion of the pelvis, vertebrae and sacrum, porous and flared rib ends and long bone metaphyses, cranial porosity, periosteal inflammatory lesions or thickening (Ortner and Putschar 1985, 275; Ortner and Mays 1989, 45). Additionally, retardation in growth can occur, which may result in shortened femora. However, bowing of long bones cannot occur if the growth is very retarded, as some bone growth needs to take place to cause bowing deformities (Stuart-Macadam 1989, 208). The bones may heal and remodel, although the frontal part of the skull and the concave surfaces of long bone deformities may remain thicker, even after years of healing (Stuart-Macadam 1989, 209). Swaddling of babies was a popular method of attempting to prevent bowing of bones (Sweet 1997, 820). However, tight bandaging could cause flesh compression and gangrene, as well as circulation disruption, thus the tradition was abandoned in the 18th and 19th centuries ibid.
Symptoms of vitamin D deficiency include restlessness, irritability, flabby muscles, pallor, gastrointestinal upsets and susceptibility to infectious disease (Stuart-Macadam 1989, 207). Females who suffered from a distorted pelvis as a result of childhood rickets often experienced very difficult and sometimes fatal births. When difficulties arose, the foetus had to be turned via internal version and extracted, resulting in its death (Rhodes 1995, 19).
Six individuals from Fishergate House exhibited different degrees of long bone bowing, the majority of which affected the lower limb bones (Table 23). A young adult male (C1128) suffered from bowing of the humeri and radii, which can occur when infants are crawling and bear most of their weight on their arms. However, there are many other possible causes for bowing deformation of long bones, including congenital anomalies and greenstick (young bone) fractures. Four individuals displayed additional skeletal lesions which may be attributed to rickets. An adolescent (C1132) had characteristic flared rib lesions, while a juvenile (C1289) had periosteal inflammatory lesions on the mandible and maxilla, and a further juvenile (C1434) had similar lesions on the right temporal. Porotic lesions on the ectocranial surface of the frontal and parietals in young adult male C1128 may have been indicative of rickets. It is possible that some of the lesions resulting from rickets had healed in the two remaining individuals (C1117, C1518); however, further indicative skeletal manifestations would be required to validate a diagnosis in these individuals.
| Context No. | Age | Sex | Location of rickets | Non-specific infection | Metabolic condition | Healed fracture |
|---|---|---|---|---|---|---|
| 1117 | 36-45 | m | bowing tibiae | periostitis on fibulae, tibia; osteitis of right tibia | Harris lines in right radius | compression fracture of right tarsals and metatarsals; avulsion fracture of right fibula; transverse fracture of left ulna, oblique fracture of left radius; os acromiale of both scapulae |
| 1128 | 20-25 | m | bowing ulnae, humeri, twisted tibiae, flattened femora | ectocranial periostitis; periostitis of tibiae | - | - |
| 1132 | 11-14 | u | bowing right fibula; flared rib ends | - | - | - |
| 1289 | 1-2 | u | bowing tibiae and right fibula | periostitis on mandible and maxilla | Harris line in right femur; cribra orbitalia | - |
| 1434 | 1-3 | u | bowing right tibia and fibula | periostitis on cranium | cribra orbitalia | - |
| 1518 | 9-11 | u | bowing femora | - | cribra orbitalia | - |
An alternative diagnosis for long bone bowing has been put forward by Stuart-Macadam et al (1998), who suggest that some bowing deformities are due to childhood trauma which, in an adult with a less supple bone structure, would have fractured the long bone. This condition, also termed 'acute plastic bowing deformity', can also be associated with inflammatory bone formation. However, the fact that no evidence for fractures or other types of trauma was noted in the group with bowed long bones suggests that rickets is the more likely cause.
Rickets is infrequently observed in medieval cemeteries; nevertheless, several cases can be found in the literature: a seven year old juvenile from St Helen's-on-the-Walls was found to have suffered from rickets, while a further case was identified in the disarticulated remains from Blackfriars. Additionally, three individuals at Jewbury were thought to have suffered from the condition. At Wharram Percy, rickets was much more prevalent, being found in eight juveniles (Ortner and Mays 1989), none of whom showed evidence for healing, suggesting that the condition in these cases was fatal. This demonstrates that although rickets was not prevalent in the medieval period, cases did occur, particularly in cemeteries associated with lower-status populations.
Scurvy is a metabolic condition caused by vitamin C deficiency and is known to have been a common problem in sailors on long voyages, frequently with fatal consequences. Scurvy is rarely seen in areas with abundant fruit resources, and is therefore more common in cooler climates, in individuals with occupations which do not allow frequent access to fresh produce, or in societies where particular cooking or eating habits reduce vitamin intake (Aufderheide and Rodríguez-Martín 1998, 310; Brickley 2000, 185). Scurvy is also often associated with hardship, famine, wars and natural disasters (Stuart-Macadam 1989, 202). A second type of scurvy, infantile scurvy (or Möller-Barlow disease) is seen primarily in infants with low birth weight, such as premature babies, or twin births, as well as infants who are fed prepared food or condensed milk ibid.
Symptoms of scurvy have been graphically described by ship's doctors and chaplains. Around 4% of vitamin C is lost daily through normal body function, and symptoms usually appear between one and three months after cessation of vitamin C intake (Aufderheide and Rodríguez-Martín 1998, 310). Contemporary accounts describe how victims' bodies were covered in ulcers, with rotting bones and flesh, and that victims suffered from swollen and bleeding gums. Long-healed wounds reopened and previously healed broken bones re-fractured, as the callous dissolved (Stuart-Macadam 1989, 202). Death was said to be sudden and unexpected.
The symptoms described included haemorrhages, infected gums and tooth loss, and in infantile scurvy, pain, immobility, enlargement and infractions of joints, susceptibility to infection, and bleeding into orbits (Stuart-Macadam 1989, 202; Brickley 2000, 185). Skeletal manifestations include periosteal inflammatory lesions of the jaw and orbits, fractures, tooth loss and enlarged long bone metaphyses (fusion sites near the long bone ends), but many of these lesions can resemble those caused by rickets and may be misdiagnosed.
Two possible cases of scurvy were identified in the Fishergate House population, both of whom showed evidence for periosteal inflammatory bone formation on the jaws and eye orbits, including woven bone deposits on the right part of the lower jaw (mandibular ramus) and on the tibiae of a young adult female (C1328), as well as porosity on the outer (ectocranial) surface of most of the cranium. She was also found to have woven bone deposits in the right orbit and supraorbital ridge. The second individual with possible scurvy was a fourteen to sixteen year old adolescent (C1143), with woven bone formation in the left orbit and on the anterior mandible, both iliae and lower legs. Neither of the individuals suffered from fractures, nor from enlarged metaphyses. The adolescent did, however, suffer from slight resorption of the bone surrounding the teeth (alveolar bone), which is unusual in individuals of such a young age, but this had not resulted in tooth loss. One further individual (C1410) showed evidence for woven bone in the left orbit, but this ten to fourteen year old juvenile showed no other possible skeletal manifestations for the condition and it was therefore not possible to diagnose scurvy. The possible presence of scurvy in the Fishergate House population suggests that part of the population were subject to inadequate nutrition, which was particularly lacking Vitamin C.
Unlike the other metabolic conditions discussed above, osteoporosis is the most common metabolic disease observed in Europe today (Roberts and Manchester 1995, 177). It is characterised by an imbalance in bone formation and resorption, causing the reduction of total bone volume, as the cortical thickness is reduced and the spongy (trabecular) bone is lost. Increasing age, gender, a diet lacking in calcium, a lack of exercise, a high number of pregnancies, prolonged lactation, smoking, caffeine, alcohol and diseases such as rheumatoid arthritis and rickets are all factors contributing to osteoporosis ibid. However, a study of osteoporosis in Britain has shown no change in bone loss over the last millennium, suggesting that changes in lifestyle are not such an important factor in the severity of osteoporosis (Mays 2000).
Two types of osteoporosis exist: primary osteoporosis, which develops in women after the menopause related to hormone changes, or senile osteoporosis which can affect both males and females, and is caused by advancing age, disease, or a reaction to drugs (Brickley 2000, 191). Osteoporotic bone loss induces greater susceptibility to fractures, especially of the femoral neck (broken hip), compression fractures of the vertebrae and fractures of the wrist (Colles fracture of the distal radius).
Six individuals from Fishergate House may have suffered from osteoporosis, although none of the skeletons were radiographed. All six individuals were female and five of these were mature adults, while the sixth was an old middle adult. However, osteoporosis was only tentatively suggested due to observed weight loss in the bones, and this could also have been caused by poor preservation of the spongy bone in the burial environment. Nevertheless, the presence of fractures in two females with possible osteoporosis may lend additional support to the diagnosis. One of these fractures was a vertebral compression fracture of the eighth thoracic vertebra (C1057), and this was the most likely case of osteoporosis. A further mature female (C1579) had numerous left and right rib fractures. It is notable that of seventeen individuals with rib fractures in this population, twelve were mature adults and four old middle adults. It is likely, therefore, that rib fractures were associated with advancing age, and may also have been related to osteoporosis. Nevertheless, twelve individuals with rib fractures were male, and merely five were female. As osteoporosis tends to have a female bias and a larger part of the mature adults from this population were female, it is likely that other factors, such as falls or fights may have contributed to the high prevalence of rib fractures in this population.
Only two of the eight vertebral compression fractures noted in this population were found in mature adults, suggesting that these fractures were not necessarily associated with advanced age and osteoporosis. A link between rickets or Harris lines and osteoporosis could not be identified. However, evidence for childhood stress was noted in only one mature female with possible osteoporosis (C1581), who had also suffered from iron deficiency anaemia.
If the prevalence rate for osteoporosis (2.5% of the population) is correct, it is slightly higher than the rates observed at Hull Magistrate's Court (1.6%) or Tarbat (1%).
Evidence for metabolic conditions was observed in a large proportion of the Fishergate House population. A total of 20% of the population (39.6% of orbits) showed evidence for cribra orbitalia, or iron deficiency. This condition can be affected by iron intake and blood loss, but has been associated predominantly with pathogen load exposure. It was found that the prevalence of metabolic conditions at Fishergate House was similar to that of other medieval populations. However, the actual prevalence of lesions in the eye orbits was greater at Fishergate House compared with other sites, and it is thought that the Fishergate House population may have been subject to greater pathogen exposure.
Harris lines were observed in the broken long bone shafts of 4% of the population. Harris lines are indicative of arrested growth during childhood and are thought to be caused by physical stress, such as childhood diseases and malnutrition. It was found that the majority of individuals with Harris lines also suffered from other conditions, such as rickets, tuberculosis, non-specific infection and cribra orbitalia. Tests to establish whether Harris lines might have affected growth concluded that this was not the case.
Rickets is caused by lack of sunlight and became prevalent in the industrial centres of Britain in the 19th century. Although medieval examples of rickets are infrequently seen, four probable (1.6%) and two possible cases (0.8%) of rickets were observed at Fishergate House.
Two possible cases of scurvy, a condition caused by lack of Vitamin C, were noted at Fishergate. This condition has not been reported from any other medieval cemeteries.
Osteoporosis is a further metabolic condition which is exacerbated by a number of factors, but is predominantly influenced by age. Six (2.4%) possible cases of osteoporosis have been observed at Fishergate House, although radiography would be required to confirm these cases and the technique, more widely applied, might detect other individuals who suffered from the condition.
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