Did children in medieval and post-medieval Poland suffer from scurvy?

Examination of the
skeletal evidence.
Marta Krenz-Niedbała; address: Institute of Anthropology, Faculty of Biology, Adam
Mickiewicz University in Poznań, Umultowska 89, 61-614, Poznań, Poland; E-mail address:
martak@amu.edu.pl; telephone +48 61 8295911; fax +48 61 8295730.

Running title: Skeletal evidence of subadult scurvy in medieval Poland

Key words: scorbutic lesions, vitamin C, metabolic disease, subadult, diet, abnormal porosity,
new bone formation, palaeopathology

Abstract
Late and post-medieval writings report that scurvy was a widespread condition in
medieval and early historical Poland. Archaeological and historical data indicate that the diet
of children was based on foods poor in vitamin C and contained small amounts of raw plant
products. Also, historians emphasize that in medieval and post-medieval Poland there were
seasonal fluctuations in food availability, frequently accompanied by poor harvests. Both
resulted in long periods of poor nutrition, which affected children most severely. The aim of
this study was to investigate skeletal manifestations of scurvy in subadult remains from
medieval and post-medieval Poland. Following standards described by Ortner et al. (1999,
2001) anatomical sites pathognomonic of scurvy in subadults (<17 years) were assessed for
abnormal porosity and hypertrophic bone among skeletons excavated from three sites:
Ostrów Lednicki (dated to the 11th-14th centuries AD), Cedynia (10th-14th centuries AD),
and Słaboszewo (14th-17th centuries AD). In total 3.6% of all examined children were found
to bear traces of vitamin C deficiency. The prevalence of scorbutic lesions was 4.5% for
Cedynia, 2.6% for Ostrów Lednicki, and 3.6% for Słaboszewo. The majority of affected
children were less than 7 years of age. Scurvy was likely more widespread in the living
populations than it appears from the calculation of skeletal markers, because some
individuals might have recovered or died before obvious traces became apparent. Also, in
some children scurvy might not have reached an advanced stage, identifiable in the skeletal
material. The prevalence of scurvy reflects not only dietary patterns but also food storage and
preparation techniques adopted in the Polish territories during the Middle Ages, which
contributed to low intakes of vitamin C.

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Introduction
Data on skeletal manifestations of inadequate vitamin intake provide important clues to
our understanding of past diet and nutrition, even though it is difficult to establish clear
criteria for recognizing osteological signs of dietary deficiencies in the skeletal remains
(Ortner et al., 2001). This is also true for scurvy, metabolic bone disease resulting from
prolonged deficiency of vitamin C - ascorbic acid, which results in defective connective
tissue and blood vessels (Aufderheide and Rodriguez-Martin, 1998; Weinstein et al., 2001;
Brickley and Ives, 2008; Mays, 2008). Humans are unable to synthesize and store vitamin C,
so they require exogenous sources, mainly fresh fruits and vegetables (Stone, 1966;
Aufderheide and Rodriguez-Martin, 1998; Ortner and Theobald, 2000; Waldron, 2009).
Vitamin C serves as a cofactor for prolyl and lysyl hydroxylases in the biosynthesis of
collagen, a major structural component of connective tissues, including bone (WHO, 1999;
Mays, 2008), while tissue and capillary vulnerability in scorbutic patients is attributed
specifically to a defect in the proline hydroxylation step of collagen formation (Pimentel,
2003).
Insufficient dietary intake of vitamin C appears as the most common cause of scurvy,
although other variables (environmental, lifestyle, biological, and pathological factors) can
contribute to the development of this disease. These variables can be categorized into four
groups: reduced intake of vitamin C (e.g. resulting from other disorders, socio-economic
factors or religious practices), increased requirement for vitamin C (e.g. during infections),
malabsorption of vitamin C (e.g. in some gastrointestinal diseases) and genetic predisposition
to lowered vitamin C levels (Delanghe et al., 2007; Halcrow et al., 2014). It was found that
genetic polymorphism of the plasma protein haptoglobin (Hp) may predispose some
individuals to scurvy. One of the three haptoglobin phenotypes, Hp 2-2, most common in
Asian populations, causes vitamin C to be more prone to oxidation than the remaining
phenotypes Hp 1-1 and Hp 2-1, This results in higher instability of vitamin C in serum, thus
the required daily intake of vitamin C in Hp 2-2 is higher compared with other Hp
phenotypes (Delanghe et al., 2007, 2011, 2013). Also, vitamin C stability in vivo may be
reduced in hemochromatosis, a disease characterized by iron overload, and associated with
populations of Celtic or Viking origin with high C282Y mutation frequency (Delanghe et al.,
2013).
Vitamin C is a relatively unstable compound, especially in neutral and alkaline
environments and when exposed to oxygen/air, heavy metals, light and heat. Also, processing
methods applied to foods, such as cooking, drying, pickling, salting, and prolonged storage
considerably lower the vitamin C content (WHO, 1999; Fain, 2005; Roberts and Manchester,
2005; Brickley and Ives, 2008; Mays 2008). Thus, the prevalence of scurvy in a given
population not only reflects dietary deficiency of vitamin C, but also food processing and
preservation methods. Historical written sources reported high frequencies of scurvy among
the inhabitants of medieval Poland (Kuchowicz, 1972), which presumably resulted partly
from poor food quality and quantity, and partly from food preparation techniques. The
purpose of this research is to identify probable cases of scurvy, a metabolic bone disease, in
subadult remains excavated from two medieval and one post-medieval cemetery of present
day Poland and to discuss possible causes for the observed pattern of lesions. Taking into
account historical records, it is expected to find a relatively high proportion of scorbutic
individuals among the medieval and post-medieval Polish children.

Childhood scurvy
Clinical manifestations
The recommended daily allowance of vitamin C is 20 mg/day for infants and 30 mg/day
for older children, while the intake should be gradually increased to adult levels as a function

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of age (WHO, 1999). In scorbutic patients treated daily with 200 mg of vitamin C, many
symptoms resolve in 3 to 5 days, and in children the complete obliteration of histological
signs of scurvy may occur after three months of vitamin C treatment (Pimentel, 2003;
Brickley and Ives, 2006).
Infantile scurvy, also called Möller-Barlow disease, is a rare condition in breastfed infants,
because the milk of well-nourished mothers contains sufficient amounts of vitamin C (WHO,
1999; Ortner, 2003; Brickley and Ives, 2008). Its prevalence increases after 4 months of age
and is highest in 8-to-10-month-old children (Ortner, 2003). Clinical symptoms of scurvy can
appear in children about 2-4 months following complete cessation of vitamin C intake
(Bourbou, 2014) and include capillary bleeding with bruising and perifollicular hemorrhages,
coiled hairs, gingival swelling and bleeding, tooth loss, subperiosteal bleeding, and muscle
and joint pains (Hodges, 1969; Hodges et al., 1971; Fain, 2005; Olmedo et al., 2006;
Waldron, 2009). A key indicator of chronic scurvy is hemorrhage, associated with trauma
either from injury or normal muscle activity leading to rupture of weakened blood vessel
walls (Brown and Ortner, 2011). Internal hemorrhages may have a destructive effect on
intestinal mucosa, brain and heart muscles, and lung physiology. The lethal effect is usually
the result of a severe infection, most commonly pneumonia (Aufderheide and Rodríguez-
Martin, 1998; Weinstein et al., 2001).

Skeletal manifestations
In the clinical view bone changes belong to the earliest and most apparent features of
subadult scurvy (WHO, 1999; Ortner, 2003). Newly formed bone often appears to be
osteopaenic (Fain, 2005; Mays, 2008). The bones that undergo rapid growth are most
severely affected, including the distal metaphysis of the femur, radius, and ulna, and the
proximal metaphysis of the humerus. The skeletal changes form directly in response to
vitamin C deficiency, and also secondarily as traumatic effects on the vulnerable bone and
associated blood vessels (Ortner, 2003). The primary lesion results from decreased
osteoblastic activity combined with continued osteo- and chondroclastic activities, leading to
the formation of calcified cartilage septa at the long bone metaphysis. This structure is highly
instable and exposed to transverse fractures (Aufderheide and Rodriguez-Martin, 1998;
Ortner, 2003; Fain, 2005).
Vascular vulnerability leads to hemorrhage, and when it occurs adjacent to bone, an
osteological response may be provoked. Even minor mechanical stress, during normal bodily
movements such as chewing, can cause the rupture of fragile blood vessels and lead to
bleeding into the skin and beneath the periosteum. Subperiosteal hemorrhages can result in
stripping of the periosteum from the bone, and as a consequence new bone may form (Ortner
and Ericksen, 1997; Ortner et al., 2001; Brickley and Ives, 2006). This is especially
symptomatic in children because of a less firm attachment of the periosteum than in adults
(Brickley and Ives, 2008). Inflammation associated with bleeding causes increased
vascularity, resulting in abnormal bone surface porosity that can develop in a variety of
locations throughout the skeleton (Ortner and Ericksen, 1997; Brickley and Ives, 2006, 2008;
Lewis, 2007).
Skeletal responses to hemorrhage, bilateral porosity and new bone formation, are the most
pathognomonic features in archaeological skeletal remains (Brickley and Ives, 2006; Brown
and Ortner, 2011). Ortner and colleagues described the broad range of skeletal manifestations
found in a series of infants and young children (Ortner and Ericksen, 1997; Ortner et al.,
1999, 2001; Ortner, 2003). This significantly contributed to an increase in the number of
palaeopathological studies of scurvy (Brickley and Ives, 2008). According to Ortner and
colleagues, the most common locations for the lesions are the external surface of the skull
vault, the orbital roof, the greater wing of the sphenoid, the posterior surface of the maxilla,

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the inferior surface of the hard palate, the infra- and supraspinous fossae of the scapula, and
the metaphyses of long bones (Ortner and Ericksen, 1997; Ortner et al., 1999, 2001; Ortner,
2003). Lesions appear to occur more frequently on the skull than on long bones (Ortner et al.,
2001), resulting from trauma to the branches of the maxillary artery that supply the
temporalis muscle, a major muscle of mastication. Pressure caused by normal contraction of
this muscle during chewing causes a sequence of events: rupture, inflammation, increased
vascularity, and bone porosity. For a description of specific anatomical relations related to the
temporalis muscle and its vasculature and an explanation of how the branches and
anastomoses of a single artery can be involved in the distribution of osteological response at
numerous anatomical sites of the skull, see Ortner and Ericksen (1997) and Table 3 in
Bourbou (2014 ).

Material
Skeletal manifestations of probable scurvy were recorded in subadults (<17 years) from
three sites located on the territory of Poland, Cedynia (dated to the 10th-14th centuries AD),
Ostrów Lednicki (11th-14th centuries AD), and Słaboszewo (14th-17th centuries AD),
representing local Latin Christian populations (Figure 1). The number of examined
individuals and age at death distributions are presented in Table 1.
Cedynia developed rapidly as a result of its favorable location along two important
medieval trade routes, one leading south of Poland down the Oder river and another leading
to the east over land (Filipowiak, 1966; Porzeziński, 2006). The cemetery was established
there at the turn of the 10th century, after a stronghold had been built in place of a former pre-
Slavonic settlement. The strategic location of Cedynia contributed to increasing trade
contacts, development of craft skills and increasing wealth of the inhabitants. In the 10th
century Cedynia became a border-fortress of high military and strategic importance. From the
end of the 11th century to the beginning of the 12th century there was a particular rapid and
dynamic economic development of the settlement, which became a metropolitan centre that
included people of high social status (Porzeziński, 2012). Its history was marked by multiple
battles. In the second half of the 13th century a series of devastating wars began that brought
poverty to the local people (Malinowska-Łazarczyk, 1982). Subsistence was based primarily
on farming and livestock, and strongly subsidized by fishing. Although the region was
abundant in forests, hunting was rather a tertiary activity of the inhabitants (Malinowska-
Łazarczyk, 1982). The cemetery is on a hill located 200 m northwest of the stronghold. The
deceased were buried according to the religious rites, along the west-east axis, in extended
and supine position (Malinowska-Łazarczyk, 1982). The cemetery served as a burial ground
for the inhabitants of both the stronghold and the surrounding urban settlement, thus the
deceased represented rather marked social stratification, starting from the members of the
magnate’s court, through merchants and craftsmen and ending with the paupers
(Malinowska-Łazarczyk, 1982; Porzeziński, 2012). Grave goods were generally scarce, and
the majority of the burials were not furnished at all. Some graves contained small amounts of
items of daily use, and there were few burials with rich grave goods. This situation resulted
partly from religious regulations that regarded grave furnishing as a pagan custom, and partly
from the fact that the buried individuals were predominantly of medium-to-low social status.
Only the period from the end of the 11th century to the beginning of the 12th century was
marked by relatively more numerous grave goods, reflecting prosperity of the site
(Malinowska-Łazarczyk, 1982). Archaeological excavations recovered approximately 1300
well preserved skeletons (Porzeziński, 2006). No orderly information is available with regard
to the exact chronology of the particular burials nor social status of the individuals buried in
Cedynia.

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 Ostrów Lednicki is the largest of five islands of the Lednica Lake, where in the 10th
century a stronghold was built. Its greatest development fell on the 10th-11th centuries. In
that time it served as one of a few residences of Polish rulers and consisted of, among others,
a palace-and-chapel complex. In the 11th century the stronghold was destroyed during an
invasion of the Czech prince Brzetysław. However, at the end of the 13th century, the entire
layout with its infrastructure was rebuilt (Górecki et al., 1994). In medieval Ostrów Lednicki
advantageous climatic conditions and fertile soils together with extensive lakeside grasslands
favored the development of agriculture (Mocek and Drzymała, 1996; Tobolski, 1991). The
subsistence was based on farming, livestock breeding, and fishing (Wrzesińska and
Wrzesiński, 2005). Archeozoological data (Makowiecki, 2001) evidence breeding of pigs
(with their predominant share in the diet), cattle, sheep, goats, geese, chicken and ducks, and
indicate a low number of wild animal remains, reflecting considerable deforestation of the
land. From 11th to 13th centuries around the Lednica Lake several servant settlements were
established to provide all necessary goods and services for the island stronghold. Faunal
analyses showed that the dwellers of the stronghold consumed higher quality meat than the
settlement inhabitants. Fish were an important food source for the elites, who followed
fasting requirements of the Christian religion (Makowiecki, 2001; Reitsema et al., 2010). The
deceased from the servant communities were buried in the local cemeteries (Górecki, 2001).
The skeletal material termed here “Ostrów Lednicki” comes from two such settlements:
Rybitwy and Dziekanowice, inhabited by craftsmen, farmers, and fishermen. The total
number of skeletons uncovered in different states of preservation exceeds 3000.
Quite different in comparison to the above mentioned sites is a small, rural village of
Słaboszewo. Unfortunately, only scarce information has been published on this population.
The inhabitants of Słaboszewo were farmers representing a typical late-medieval local
society (Piontek, 1981) that lived a rather harsh but stable life far from important trade routes.
In the second half of the 14th century the Słaboszewo parish consisted of 288 people, and
occupied an area of 38.9 km2 (Piontek, 1977). Archaeological excavations carried out in the
19th and 20th centuries uncovered approximately 600 skeletons associated with the remains
of a church dating to the 14th to 17th centuries.

Methods
Age at death of the examined subadults was determined on the basis of dental
development and eruption, bone lengths, and the degree of epiphyseal fusion (Scheuer and
Black, 2000, 2004; Schaefer et al., 2009; White et al., 2012). The study included the
skeletons with at least 60% of bones preserved and represented by both cranial and post-
cranial elements.
Scurvy was diagnosed according to Ortner et al.'s (1997, 1999, 2001) criteria. The
following anatomical sites associated with scorbutic lesions were examined for abnormal
porosity and hypertrophic bone formation (Ortner et al., 2001; Lewis, 2007): cranial vault
(external table), greater wing of sphenoid, orbital roof, orbital and internal aspects of
zygomatic bone, posterior aspect of maxilla, infraorbital foramen, palate, medial coronoid
process of mandible, supraspinous and infraspinous fossae of scapula, and metaphyses of
long bones. Abnormal porosity was defined after Ortner et al. (2001) as a localized condition,
in which holes less than 1 mm in diameter penetrate a compact bone surface. Distinguishing
abnormal from normal porosity of posterior maxilla and hard palate poses problems, because
these anatomical sites involve vascular response to erupting teeth. Abnormal porosity was
diagnosed according to Ortner et al.’s (1999) criteria. For the maxilla it was recorded when
the area of porous involvement extended beyond the alveolar process surrounding molars,
and for the palate it was diagnosed when dense porosity extended onto the posterior portion
of the hard palate. Pathological porosity of metaphyses was distinguished from porosity

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associated with normal metaphyseal remodeling on the basis of the size of the affected area,
extending more than a centimeter from the end of the bone (Ortner et al., 1999). Hypertrophic
bone formation, although less frequent in scurvy than porotic lesions, was also recorded
following Ortner et al.'s suggestions, as being superficial to existing compact bone. Each
lesion was evaluated in terms of being active, healing or healed basing on the presence or
lack of remodeling (Brown and Ortner, 2011; Mays, 2014). For all available anatomical sites
the lesions were scored as absent, present or nonobservable. Following Ortner’s approach, the
prevalence of scorbutic individuals was calculated using only those skeletons on which at
least one greater wing of the sphenoid bone was observable (Ortner et al., 1997, 1999, 2001).
Preliminary data on the frequencies of scorbutic individuals in the skeletal series
included in the present study have been previously published in a paper on skeletal health and
growth of subadults from Ostrów Lednicki (Krenz-Niedbała, 2009). For the purpose of the
present study all cases were reevaluated according to the diagnostic criteria of Geber and
Murphy (2012). This approach was applied, because the skeletons were partial and
fragmented, as it is common for subadult remains, and because of the generally nonspecific
nature of skeletal indicators of scurvy. Geber and Murphy (2012), aiming at more consistent
diagnosis across the whole sample (to include also incomplete skeletons) used statistical
correlation analyses to group different combinations of lesions into definite, probable and
possible diagnoses. Thus, the anatomical sites listed in the previous paragraph were
categorized into definite, indicative and suggestive variables, according to Geber and
Murphy’s (2012) criteria. Definite diagnoses were made when abnormal porosity/new bone
was found within the anatomical sites involved in mastication and tooth eruption regarded as
pathognomonic of scurvy (Ortner et al., 2001; Brickley and Ives, 2008; Geber and Murphy,
2012): greater wing of sphenoid, posterior aspect of maxilla, medial coronoid process of
mandible, and palate. Probable scurvy was recorded in the case of lesions observed on orbital
and internal aspects of the zygomatic bone, infraorbital foramen, supraspinous fossa of
scapula, and metaphyses of long bones. Lesion combinations suggestive of scurvy were
recorded on the basis of abnormal porosity and/or new bone formation observed on the
cranial vault, orbital roof, and infraspinous fossa of scapula (Geber and Murphy, 2012). The
prevalence of scurvy were then calculated taking into account all individuals with traces of
the disease, and, unlike in the Ortner’s approach, the presence of the greater wing of the
sphenoid bone was not the necessary condition for the individuals to be included in the
analysis.

Results
Age-at-death
Table 1 presents age at death distributions in the total examined set of skeletons and
separately for Cedynia, Ostrów Lednicki, and Słaboszewo. These three distributions are
similar in terms of the percentage of individuals deceased in particular age categories. For the
total sample, children aged between 2.6 and 6.5 years make up the largest group (28.9%), and
the 6.6-10.5-year-olds make up the second largest age category (25.3%). This is true also for
each population taken separately. The lowest number of subadults died before 6 months of
age (4.3%), followed by the oldest individuals, 14.6-17.0-year-olds (9.5%).

Palaeopathological evidence for scurvy

Of the 506 individuals examined, 18 (3.6%) showed any type of abnormal porosity and/or
active hypertrophic changes consistent with the lesions described in the definite, indicative
and/or suggestive categories (Table 2). These lesions were apparent on 4.5% of the skeletons
(n=9) at Cedynia, 2.6% (n=5) of the skeletons at Ostrów Lednicki, and 3.6% of the skeletons
(n=4) from Słaboszewo. The results based on Ortner’s approach (including only those

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individuals who were represented by at least one greater wing of the sphenoid bone) proved
relatively similar to the ones for the total sample (Table 2). Of the 267 individuals, 12 (4.5%)
had lesions attributed to scurvy. The differences between these two approaches at least partly
result from a decreased number of skeletons used in the Ortner’s approach (requiring the
presence of the greater wing of the sphenoid bone), most apparent for the Słaboszewo
sample. The slight differences in the frequencies of scorbutic children between the three
studied populations proved nonsignificant in Chi-square tests at p-level 0.05. The affected
subadults are included in the age category of 0.6-14.5 years. Table 3 shows that half of them
are between 9 months and 3 years of age and the next six individuals are between 4 and 7
years of age.
Table 3 presents detailed observations in the three samples examined. The anatomical sites
were grouped into definite, indicative and suggestive variables and designated as having/not
having abnormal porosity and/or hypertrophic bone formation. Table 3 demonstrates that
abnormal porosity, when present, typically affects multiple anatomical sites pathognomonic
of scurvy. Thus the observations in this study confirm the approach of Geber and Murphy
(2012), in which the variables were divided according to their diagnostic value, because when
abnormal porosity or hypetrophic lesions were found for definite variables, in the majority of
individuals they were also present for the indicative ones, and also for some suggestive ones.
The least diagnostic in this study seem to be the lesions found on the cranial vault and
infraspinous fossa of the scapula being designated as suggestive for scurvy, since in some
cases they were not observed, despite the involvement of the definite traits. A definite
diagnosis of scurvy was made for all but one of the skeletons showing lesions (Słaboszewo
127/35). This specimen was represented only by postcranial bones, scapulae and long bones,
and abnormal porosity was found only on long bone metaphyses.
The lesions were typically bilateral, which was observed in all cases when both right and
left bone elements were available. As expected, abnormal porosity was more frequent than
new bone formation, with the latter recorded in 28.3% of lesions (hypetrophic changes
accompanied 26 of the total of 92 porotic lesions) (Table 3). Figures 2-6 display examples of
porosity and hypertrophic bone attributable to scurvy found in the examined subadults. All
but one lesion (Fig. 3A – healing lesion of the orbital roof) were found to be active, which
suggests that the vitamin C deficiency was active at time of death.

Differential diagnoses
There are three diseases resulting from nutritional deficiency, rickets (vitamin D
deficiency), iron-deficiency anemia, and scurvy (vitamin C deficiency), which tend to co-
occur in the same individual, because of their underlying relationship to malnutrition (Ortner
et al., 1999). Because they may cause bony changes similar to the ones observed in this
study, both rickets and anemia need to be taken into account in differential diagnoses. Other
potential conditions to be considered include chronic non-specific infection, treponemal
disease, and bone-forming disorders, i.e. secondary hypertrophic osteoarthropathy and
infantile cortical hyperostosis (Klaus, 2014). Chronic infection leads to periosteal
inflammation and pathological new bone formation in form of plaque-like, rather superficial
and localized, patches of bone raised above the original cortex (Ortner, 2003). The most
common anatomical site for this lesion is the anterior medial surface of the tibial diaphysis
(Ortner, 2003; Lewis, 2007). It is rather unlikely that the observed bony changes are due to a
non-specific infection, since they lack the plaque appearance and elevation, and they are
closely associated with muscle attachments and movement.
Congenital or acquired treponemal disease also cannot be responsible for the lesions
observed, because no changes typical of this condition have been found, such as saber shin
deformity, cortical thickening of long bones, crater-like lesions of the skull vault (caries

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sicca) or dental defects, which are currently regarded as pathognomonic of congenital
syphilis (Lewis 2007).
Secondary hypertrophic osteoarthropathy (HOA) is a bone-forming disorder that can
produce postcranial new bone resembling the lesions produced by scurvy (Aufderheide and
Rodríguez-Martin, 1998; Ortner, 2003). The new bone is usually thickest at mid-diaphysis,
tapering toward the metaphysis, while the epiphyses and tendon insertions are spared
(Aufderheide and Rodríguez-Martin, 1998; Ortner, 2003), which is in contrast to the
locations of postcranial new bone formation seen in the cases examined here. No changes
typical of HOA have been observed in this study, including diaphyseal thickening and
remodeling changes consistent with clubbing of fingers and toes. Moreover, the bones of the
skull are affected, while in HOA they are unchanged, apart from bone deposition on the inner
table (Aufderheide and Rodríguez-Martin, 1998). This comes as no surprise, since children
are rarely affected by the disorder.
Another bone-forming disease causing lesions similar to scurvy is infantile cortical
hyperostosis (ICH), or Caffey’s disease. It involves the bones of both the skull and
postcranial skeleton, causing periosteal inflammation and local cortical thickening. Usually it
manifests as an isolated, asymmetrical lesion located on the mandible, the clavicle and long
bones being indicative of the disorder (Aufderheide and Rodríguez-Martin, 1998). A
differential diagnosis of ICH can be rejected, because the pattern of lesions does not fit the
one observed in ICH. No unilateral and localized changes of mandible and clavicle have been
recorded. Also, the metaphyses and skull are spared in this condition, in contrast to the
findings in this study (Aufderheide and Rodríguez-Martin, 1998; Ortner, 2003).
Metabolic diseases, such as rickets (vitamin D deficiency) can cause deposits of porous
periosteal bone that closely resemble scorbutic lesions (Ortner and Mays, 1998; Ortner, 2003;
Brickley and Ives, 2008). However, in the cases observed here there is an absence of changes
typical of rickets, such as bending abnormalities of long bones, rachitic rosary (bowing,
cupping and flaring deformities of the rib cage), and skull or pelvic deformation. Another
condition that needs to be considered is chronic anemia, which leads to expansion of red bone
marrow contained in diploë in response to the need of the body to produce and store more red
blood cells. This process occurs at the expense of the outer table causing porous appearance
of the cranial bones (Ortner et al., 2001; Ortner, 2012). However, the lesions of the cranial
vault and orbital roof observed in this study lack evidence of marrow hyperplasia.
Additionally, in all cases with the sphenoid bone present, the greater wing shows porosity,
which is unlikely to develop under anemic conditions on account of its minimal marrow
space (Ortner and Ericksen, 1997; Armelagos et al., 2014; Klaus, 2014).
In each case the pattern of lesions argues for a diagnosis of scurvy. There is no other
pathological condition of the skeleton known to produce a combination of abnormal porosity
of the greater wing of the sphenoid bone (considered to be pathognomonic of scurvy) and of
other involved cranial sites, and new bone formation associated with the location and activity
of muscles involved in mastication and movement of limbs (Ortner and Ericksen, 1997;
Ortner et al., 2001; Klaus, 2014).

Discussion
The frequencies of lesions likely due to scurvy found in the present study conform to the
results of other studies on subadults from medieval and post-medieval Europe with
prevalences ranging from 0 to approximately 7% (Brickley and Ives, 2008: Table A1, pp 72-
74; Mays, 2014: Table 2). However, scurvy may prove much more prevalent both in
disadvantageous circumstances, like famine (Geber and Murphy, 2012) or, on the contrary, in
wealthy communities (Pētersone-Gordina et al., 2013). So far only one study has been
published on childhood scurvy in medieval Poland. The skeletal remains came from a

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cemetery in Giecz, dated to the 11th-12th centuries AD. Only one of 85 subadult skeletons
exhibited lesions consistent with scurvy (Agnew et al., 2008).
Based on nonsignificant differences in the frequencies of scorbutic children between the
three studied populations it appears that the type of settlement (urban centre of Cedynia and
servant settlements of Ostrów Lednicki versus the post-medieval village of Słaboszewo) did
not influence the level of vitamin C deficiency, thus it may be inferred that the childhood diet
composition with regard to this vitamin content did not much differ between the examined
sites. The vitamin C status in the Polish territories seems to have been generally poor, and
improved only with the widespread consumption of potatoes starting in the 19th century
(Leszczyński, 2012). In general, the frequency of scurvy in the living subadults was
presumably higher than calculated on the basis of skeletal markers. In children it takes a few
months (between 2 and 6) of inadequate intake of vitamin C to develop recognizable signs of
the disease (Ortner, 2003; Bourbou, 2014), and some individuals might have recovered or
died (for example of acute infections) before obvious traces became apparent (Brickley and
Ives, 2008; Armelagos et al., 2014;, Mays, 2014). Also, in some individuals scurvy might not
have been sufficiently advanced to be identified in the skeletal material. Those with no bone
lesions may have been in fact the ones most severely affected by the disease, being too weak
to survive long enough to display skeletal traces. This issue is well known in anthropology
under the name of the “osteological paradox” (Wood et al., 1992). A reflection of the paradox
in a 19th century population deprived of vitamin C was observed by Geber and Murphy
(2012). They found greater frequencies of non-scorbutic individuals than scorbutic ones
among newborns and infants. On the contrary, in older age categories a higher mortality rate
was found for skeletons with scurvy. The authors claim that many youngest children had died
before skeletal lesions had time to develop. Thus, care is required when inferring the true
prevalence of scurvy from skeletal markers.
The youngest individual affected by vitamin C deficiency is 9 months old. This vitamin
passes to infants through their mother's breastmilk, thus breastfed infants typically do not
develop scurvy. Infantile scurvy may occur in artificially fed children or if breastfeeding
mothers are deficient in vitamin C (Fain, 2005), as it could have been the case for the 9-
month-old infant. Weaning in medieval Poland was complete by 2-3 years, although it was
not an abrupt process, but associated with a gradual introduction of solid foods (Tyszkiewicz,
1983; Żołądź-Strzelczyk, 2002; Delimata, 2004). By 9 months of age infants would have
received food in addition to their mother's milk. As described below, such complementary
food was very low in vitamin C. Chewing solid foods or habitual chewing of non-food
objects during teething (Ortner and Mays, 1998) likely caused sufficient mechanical stress to
masticatory muscles to cause bleeding and inflammatory response. The general age pattern of
scurvy in subadults is variable, depending on the population studied, with infants and young
children more likely to develop defective blood vessels and show skeletal manifestations of
scurvy than adolescents due to their rapid growth (Ortner et al., 2001; Brickley and Ives,
2006). This is supported by the results of this study, where almost all cases ranged between
the 1st and 7th years of age. However, scurvy seems to have persisted into late childhood,
similarly to a Late Romano-British settlement examined by Lewis (2010) or to a Latvian 17-
18th century German community studied by Pētersone-Gordina et al. (2013), where scorbutic
lesions were found also in a 17-19-year-old individual.
Hypertrophic lesions (N=26) were found to be less frequent than porotic lesions (N=92)
(Table 3). As ossification of new bone in areas of subperiosteal bleeding requires some
vitamin C to start the osteoid formation (Brickley and Ives, 2008; Klaus, 2014), it seems that
small amounts of this vitamin must have been occasionally ingested by the affected
individuals. This appears probable, as the complete exclusion of vitamin C from the human
diet is rare (Brickley and Ives, 2008; Klaus, 2014), and the intake in the climatic conditions

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of the Polish territories is season-dependent. Thus, it is likely that the examined subadults at
times consumed food containing some vitamin C.
In some human societies there may be a genetic predisposition to low levels of vitamin C,
for example in the populations of Celtic or Viking origin or in Asian populations (Delanghe
et al., 2013; Halcrow et al., 2014). However, the idea that genetic factors contributed to
scurvy development in the examined samples is rather unlikely, because of their European
Slavic origin. Since the most common cause of scurvy is insufficient dietary intake of vitamin
C, most cases of scorbutic lesions in archaeological samples are attributed to an inadequate
diet (Lovász et al., 2013; Halcrow et al., 2014), with a possible strong influence of religious
and child-rearing practices (Lewis, 2010). Although scurvy has historically occurred under
diet-restriction circumstances, such as long sea voyages (Aufderheide and Rodriguez-Martin,
1998; WHO, 1999; Maat, 2004; Brown and Ortner, 2011), it seems that vitamin C deficiency
occurred quite frequently in the past (Ortner et al., 2001; Brickley and Ives, 2008) and
remains common today (Maat, 2004; Fain 2005). Scurvy has been endemic in northern and
temperate climates during late winter months due to the unavailability of fresh vegetables
(WHO, 1999; Maat, 1986: 160, after Ortner and Theobald, 2000) and is assumed to have
been more prevalent in settled agricultural societies, where limited gathering of fresh fruits
and consumption of staple crops would have contributed to low vitamin C intake (Roberts
and Manchester, 2005). Melikian and Waldron (2003) state that scurvy was likely to have
shown considerable seasonal variation in the past, being most prevalent in the seasons when
fresh fruit and vegetables were least available, which was shown in several studies on
medieval European populations. Elevated prevalence of subadult scurvy (35.8%), attributed
to seasonal shortages of fresh fruit and vegetables, was found for a medieval population from
Straubing, Germany (Kreutz, 1997, after Schultz 2001), though in this case there is some
controversy related to the methods of scurvy diagnosis used by the author and her associates
(see Mays, 2014). Mahoney-Swales and Nystrom (2009) found it possible that the scorbutic
children in their Early Medieval British sample died during late winter or early spring, before
they had time to recuperate from skeletal effects of vitamin C deficiency. Not only
seasonality, but also socio-economic factors may have predisposed individuals to scurvy in
the Middle Ages. The diet of working-class people prior to the 16th century, mainly based on
grains supplemented with salted and/or dried meat or fish and very small amount of fresh
fruits and vegetables, is presumed to have caused widespread scurvy (Prentice, 1939, after
Hughes, 2000).
Historical written sources emphasized high frequencies of scurvy in late medieval and
early historical Poland, reporting on Polish people's "organic susceptibility" to this disease
(Kuchowicz, 1972). Numerous antiscorbutic information and medicines were published in
medical guides and herbals, and also many real and quack doctors advertised themselves
claiming to be able to cure scurvy. Death records from the 18th/19th centuries even listed
scurvy among the causes of death. Historians assume that scurvy was common in two
contrasting social groups, members of the upper social class, because of their limited diet,
based on meat, fat and alcohol, and among the poorest people, because of general
undernutrition (Kuchowicz, 1972). Much later, scurvy prevalence decreased as a
consequence of widespread cultivation of potatoes, which became a basic staple at the
beginning of 19th century (Leszczyński, 2012). Unfortunately, little is known about the food
consumption in Cedynia and Słaboszewo - only the Ostrów Lednicki site has been thoroughly
examined in terms of archeozoology (Makowiecki, 2001) and archeobotany (Polcyn, 2003;
Reitsema et al., 2010). Thus, the data from historians on eating habits in the Polish Middle
Ages (Dembińska, 1963, 1999), and information provided by research of plant and animal
remains in medieval Poland in general and Ostrów Lednicki in particular, served as a basis
for consideration of the diet in this study.

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 Written evidence related to daily life including food consumption in medieval Poland is
scarce, especially in relation to the middle class and the poor. What is known to
archaeologists and historians on the early Medieval Times is derived almost entirely from
archaeological findings (Dembińska, 1999). The common approach in food history research
is to divide the medieval society into four social groups: nobility, clergy, townspeople, and
peasants, but it does not work for understanding the real differences in eating habits in the
Polish Middle Ages, because the quality and quantity of food consumed were determined by
the standard of living rather than those arbitrary categorizations (Dembińska, 1999). In fact
each social group was diverse. To the nobility, apart from royalty, magnates and nobles, also
belonged state and court officials (not always of noble origin), and persons closely associated
with the court. The clergy group embraced rich (including landed prelates) and poor priests,
monks and friars, and the lowest rank of monks of peasant origin. Also, to medieval
townspeople belonged urban patricians, middle-class merchants, craftsmen, and the urban
poor. The peasantry living in the countryside ranged from village administrators and rich
farmers to middle-class peasants, rural craftsmen to herdsmen, tenants, rural poor, beggars
and vagabonds. Therefore, similar eating patterns are expected to have been shared by the
people of comparable standard of living. The highest group in the consumption hierarchy
consisted of secular and church magnates, royalty, wealthy nobles, court officials, rich
patricians, and their servants, minor officials, state clerks etc. The next group embraced
landowners of small estates, knights, middle-class merchants, craftsmen, village
administrators, wealthy farmers, and the middle-income clergy. To the third, lowest, category
belonged, among others, urban and rural poor, friars, and low-level servants. This group was
numerous in medieval Poland, though invisible in the written records (Dembińska, 1999).
In medieval Poland there was a general belief that quantity of food was more important
than the type of food, although meat had the highest value. The most frequently consumed
meats were pork (because of the features of pig farming, i.e. easy foddering and rapid
reproduction), and beef, then poultry. Offal, while it is not known what specific organs were
eaten, was considered food for the poor. Fish were an important food source for the elites
who followed religious practices, because they substituted meat on fasting days. For storage
purposes meat and fish were dried, salted, smoked, or pickled. Dairy products (milk, butter,
cheese, eggs) were only minor parts of the diet (Dembińska, 1963; Kuchowicz, 1972).
Cereals remained the most important staples. Grains, primarily millet, cooked in water
with butter and salt, were the primary constituent of most meals, with boiled peas, parsley,
and cabbage (cooked or pickled in brine) being the most common vegetables. Millet formed a
key element of everyday diet prior to the introduction of the potato, because of favorable
climatic conditions and its adaptability to the slash-and-burn farming of medieval Poland.
This was one of the distinctive features of medieval Polish cookery that differentiated it from
cookery in Western and Northern Europe (Dembińska, 1999; Reitsema et al., 2010). Findings
of pollen and carbonized seeds of proso millet recovered from early medieval sites in the
Polish territory (Reitsema et al., 2010) support the information from medieval documents on
millet widespread consumption. Raw plant products were generally lacking in the medieval
Polish diet (Dembińska, 1963). Vegetables were always cooked. Only fruits were eaten raw,
but they were mostly dessert foods of the rich, because of their highly limited cultivation
(Dembińska, 1963; Kuchowicz, 1972; Polcyn, 2003; Dembińska, 1999). These historical data
are very important for the interpretation of the prevalence of scurvy, because the populations
that consume only cooked foods are highly susceptible to vitamin C deficiency (Ortner et al.,
2003).
The diet composition was largely determined by social class and age (Table 4). The
amount of meat one ate was a measure of well-being, thus it is not surprising that the meals
of upper class people were based on meat, and fat, and the portions of food were generally

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larger (Tyszkiewicz, 1983), while infants and young children were given paps of porridge or
bread with milk or water. For the majority of the lower class people, peasants and workers, a
large portion of their daily diet was made up of grains such as millet, wheat, oats or barley.
Lower class children consumed the same but crushed food as their parents. In general,
subadults’ diet was limited, based on a few products, containing no or small amounts of
vitamin C (Table 4). Children aged 4-5 years started to be given adult food (Żołądź-
Strzelczyk, 2002). Thus, both high-status and low-status children were exposed to vitamin C
deficiency. Importantly, in Poland winters are long and the growing season for vegetables
and fruits does not start until mid-June. Seasonal fluctuations in food availability and poor
harvests often caused long periods of very poor nutrition, which most severely must have
affected the children, belonging to the most vulnerable sections of a population (Żołądź-
Strzelczyk, 2002; Lewis, 2007; Pētersone-Gordina et al., 2013).
Ortner et al. (2001) showed that scurvy can develop also in sub-tropical areas despite
abundant vitamin C rich foods, due to destruction of the vitamin during cooking or an
overreliance on vitamin C-deficient foods. Mays (2008) also suggested cooking practices to
be responsible for scurvy. Vitamin C in food is unstable in neutral and alkaline environments
and when exposed to oxygen/air, heavy metals (iron, copper), and light and heat (WHO,
1999), thus adverse conditions of storage and preparation substantially decrease this vitamin
content. Prolonged storage of fruits and vegetables cause heavy losses of vitamin C through
enzymatic decomposition. Processing of food, e.g. by salting, smoking, drying, and
prolonged cooking, is also detrimental to vitamin C retention. Minimum losses are about 50%
during long, slow cooking and slow cooling (WHO, 1999). Thus, with regard to food storage
and processing (Table 4) high losses of vitamin C must have occurred in medieval and post-
medieval Poland.
Taking into account archaeological and historical data, including documentary sources, it
was expected to find a relatively high prevalence of scorbutic children in this study. The
obtained frequency of c. 4% appears neither high nor low compared with other medieval
European populations (Brickley and Ives, 2008: Table A1, pp 72-74; Mays, 2014: Table 2).
Thus, it is possible that historical accounts of particular susceptibility of inhabitants of
medieval and post-medieval Poland to scurvy were exaggerated, and maybe other disorders
(e.g. periodontal diseases) were mistaken for this disease. Generally, basing on the findings
from this study it may be inferred that the dietary status of medieval Polish children
corresponded to other European sites in the Middle Ages. It seems that the most likely
underlying causes of scurvy in the examined subadults would be cultural rather than
environmental variables, including restricted childhood diet, significant reliance on foods
deficient in vitamin C, low consumption of raw products, and food preservation and
preparation methods, based on cooking the food (see Mays, 2014). However, limitations of
skeletal research in terms of representativeness and taphonomic effects should be borne in
mind when comparing results from different studies.

Conclusions
This paper provides skeletal evidence that children in medieval/early historical Poland did
suffer from vitamin C deficiency. Late and post-medieval writings indicate that scurvy was a
widespread condition, mainly affecting two contrasting social groups – higher class members
and the poorest people. Diet likely played a role in the development of the disease, because it
lacked raw plant products. Historical data emphasize that subadult food, particularly in early
childhood, was strongly limited, based only on a few products containing no or low amounts
of vitamin C. Food storage and processing procedures presumably contributed to vitamin C
deficiencies in the examined populations. Also, seasonal fluctuations in food availability and

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frequent poor harvests caused long periods of very poor nutrition, that were detrimental to
children.

Acknowledgements
The author is very grateful to Professor J. Piontek from the Institute of Anthropology Adam
Mickiewicz University in Poznań, Poland and to A. Wrzesińska and J. Wrzesiński from the
Museum of the First Piast at Lednica, Poland for the access to the skeletal material. The
author also would like to thank the anonymous reviewers for their effort, and for the thorough
comments and corrections, which significantly contributed to improving the quality of the
paper.

References
Agnew AM, Justus HM, Stout SD. 2008. Evidence of scurvy in medieval Eastern Europe: A
possible case from Giecz, Poland. http://www.slavia.org/posters/2008_ppa.pdf.
Armelagos GJ, Sirak K, Werkema T, Turner BL. 2014. Analysis of nutritional disease in
prehistory: The search for scurvy in antiquity and today. International Journal of
Paleopathology: 5: 9-17.
Aufderheide AC, Rodríguez-Martín C. 1998. The Cambridge encyclopedia of human
paleopathology. Cambridge: Cambridge University Press.
Bourbou C. 2014. Evidence of childhood scurvy in a Middle Byzantine Greek population
from Crete, Greece (11th –12th centuries A.D.). International Journal of Paleopathology: 5:
86-94.
Brickley M, Ives R. 2006. Skeletal manifestations of infantile scurvy. American Journal of
Physical Anthropology 129: 163–172. DOI: 10.1002/ajpa.20265.
Brickley M, Ives R. 2008. The bioarchaeology of metabolic bone disease. Academic Press:
London.
Brown M, Ortner DJ. 2011. Childhood scurvy in a medieval burial from Macvanska
Mitrovica, Serbia. International Journal of Osteoarchaeology 21: 197–207. DOI:
10.1002/oa.1124.
Delanghe JR, De Buyzere ML, Speeckaert MM, Langlois MR. 2013. Genetic aspects of
scurvy and the European famine of 1845-1848. Nutrients 5: 3582-3588. DOI:
10.3390/nu5093582.
Delanghe JR, Langlois MR, De Buyzere ML, Na N, Ouyang J, Speeckaert MM, Torck MA.
2011. Vitamin C deficiency: more than just a nutritional disorder. Genes & Nutrition 6: 341-
346. DOI: 10.1007/s12263-011-0237-7.
Delanghe JR, Langlois MR, De Buyzere ML, Torck MA. 2007. Vitamin C deficiency and
scurvy are not only a dietary problem but are codetermined by the haptoglobin
polymorphism. Clinical Chemistry 53: 1397-1400. DOI: doi: 10.1373/clinchem.2007.088658.
Delimata M. 2004. Dziecko w Polsce średniowiecznej. Wydawnictwo Poznańskie: Poznań.
Dembińska M. 1963. Konsumpcja żywnościowa w Polsce średniowiecznej. Zakład Narodowy
im. Ossolińskich, PAN: Wrocław-Warszawa-Kraków.
Dembińska M. 1999. Food and drink in medieval Poland. Rediscovering a cuisine of the
past. University of Pennsylvania Press, Philadelphia.
Fain O. 2005. Musculoskeletal manifestations of scurvy. Joint Bone Spine 72: 124–128. DOI:
10.1016/j.jbspin.2004.01.007.
Filipowiak W. 1966. Cedynia w czasach Mieszka I. Wydawnictwo Poznańskie: Poznań.

This article is protected by copyright. All rights reserved.

Geber J, Murphy E. 2012. Scurvy in the Great Irish Famine: evidence of vitamin C deficiency
from a mid-19th century skeletal population. American Journal of Physical Anthropology
148: 512–524. DOI: 10.1002/ajpa.22066.
Górecki J. 2001. Gród na Ostrowie Lednickim na tle wybranych ośrodków grodowych
pierwszej monarchii piastowskiej. Biblioteka Studiów Lednickich VII: Lednogóra.
Górecki J, Łastowiecki M, Wrzesiński J. 1994. Wczesnośredniowieczne budownictwo
mieszkalne Ostrowa Lednickiego. Studia Lednickie 3: 21–45.
Halcrow SE, Harris NJ, Beavan NJ, Buckley HR. 2014. First bioarchaeological evidence of
probable scurvy in Southeast Asia: Multifactorial etiologies of vitamin C deficiency in a
tropical environment. International Journal of Paleopathology 5: 63–71. DOI:
10.1016/ijpp.2014.01.004.
Hodges RE. 1969. Experimental scurvy in man. American Journal of Clinical Nutrition 22:
535–548.
Hodges RE, Hood J, Canham JE, Sauberlich HE, Baker EM. 1971. Clinical manifestations of
ascorbic acid deficiency in man. American Journal of Clinical Nutrition 24: 432–443.
Hughes RE. 2000. Scurvy, In The Cambridge world history of food, Kiple KF, Ornelas KC
(eds). Cambridge University Press, 1: 988–1001.
Klaus HD. 2014. Subadult scurvy in Andean South America: Evidence of vitamin C
deficiency in the late pre-Hispanic and Colonial Lambayeque Valley, Peru. International
Journal of Paleopathology: 5: 34-45.
Krenz-Niedbała M. 2009. Skeletal health and growth indicators in medieval children from
Ostrów Lednicki, western-central Poland. Anthropologie: XLVII/3: 255–265.
Kuchowicz Z.1972. Z badań nad stanem biologicznym społeczeństwa polskiego od schyłku
XVI do końca XVIII wieku. Łódzkie Towarzystwo Naukowe, Polska Akademia Nauk 74:
Łódź.
Leszczyński W. 2012, Żywieniowa wartość ziemniaka i przetworów ziemniaczanych
(przegląd literatury). Biuletyn Instytutu Hodowli i Aklimatyzacji Roślin 266: 5–20.
Lewis M. 2007. The bioarchaeology of children: Perspectives from biological and forensic
anthropology. Cambridge: Cambridge University Press.
Lewis ME. 2010. Life and death in a civitas capital: metabolic disease and trauma in the
children from late Roman Dorchester, Dorset. American Journal of Physical Anthropology
142: 405–416. DOI: 10.1002/ajpa.21239.
Lovász G, Schultz M, Gödde J, Bereczki Z, Pálfi G, Marcsik A, Molnár E. 2013. Skeletal
manifestations of infantile scurvy in a late medieval anthropological series from Hungary.
Anthropological Science 121: 173–185. DOI: 10.1537/ase.130905.
Maat GJR. 2004. Scurvy in adults and youngsters: The Dutch experience. A review of the
history and pathology of a disregarded disease. International Journal of Osteoarchaeology
14: 77–81. DOI: 10.1002/oa.708.
Mahoney-Swales D, Nystrom P. 2009. Skeletal manifestation of non-adults scurvy from
Early Medieval Northumbria: The Black Gate Cemetery, Newcastle-upon-Tyne. In
Proceedings of the 9th Annual Conference of the British Association for Biological
Anthropology and Osteoarchaeology, Lewis ME, Clegg M (eds). University of Reading.
BAR International Series 1918: 31–41.
Makowiecki D. 2001. Hodowla oraz użytkowanie zwierząt na Ostrowie Lednickim
w średniowieczu. Studium archeozoologiczne. Biblioteka Studiów Lednickich 6: Poznań.

This article is protected by copyright. All rights reserved.

Malinowska-Łazarczyk H. 1982. Cmentarzysko średniowieczne w Cedyni. Muzeum
Narodowe w Szczecinie.
Mays S. 2008. A likely case of scurvy from Early Bronze Age Britain. International Journal
of Osteoarchaeology 18:178–187. DOI: 10.1002/oa.930.
Mays S. 2014. The palaeopathology of scurvy In Europe. International Journal of
Paleopathology: 5: 55-62.
Melikian M, Waldron T. 2003. An examination of skulls from two British sites for possible
evidence of scurvy. International Journal of Osteoarchaeology 13: 207–212. DOI:
10.1002/oa.674.
Mocek A, Drzymała S. 1996. Zróżnicowanie gleb a kierunki produkcji rolnej w Lednickim
Parku Krajobrazowym. Studia Lednickie 3: 79–88.
Olmedo JM, Yiannias JA, Windgassen EB, Gornet NK. 2006. Scurvy: a disease almost
forgotten. International Journal of Dermatology 45: 909–913.
Ortner D. 2003. Identification of pathological conditions in human skeletal remains. Second
edition. San Diego: Academic Press.
Ortner DJ. 2012. Differential diagnosis and issues in disease clarification. In A Companion to
Paleopathology, Grauer AL (ed.). Willey-Blackwell, Chichester, UK, pp. 250–267.
Ortner DJ, Butler W, Cafarella J, Miligan L. 2001. Evidence of probable scurvy in subadults
from archeological sites in North America. American Journal of Physical Anthropology 114:
343–351.
Ortner DJ, Ericksen MF. 1997. Bone changes in the human skull probably resulting from
scurvy in infancy and childhood. International Journal of Osteoarchaeology 7: 212–220.
Ortner DJ, Kimmerle EH, Diez M. 1999: Probable evidence of scurvy in subadults from
archeological sites in Peru. American Journal of Physical Anthropology 108: 321–331.
Ortner D, Mays S. 1998. Dry-bone manifestations of rickets in infancy and early childhood .
International Journal of Osteoarchaeology 8: 45–55 .
Ortner DJ, Putschar W. 1981. Identification of pathological conditions in human skeletal
remains. Washington: Smithsonian Institution Press.
Ortner DJ, Theobald G. 2000. Paleopathological evidence of malnutrition. In The Cambridge
world history of food, Kiple KF, Ornelas KC (eds). Cambridge University Press 1: 34–44.
Pētersone-Gordina E, Gerhards G, Jakob T. 2013. Nutrition-related health problems in a
wealthy 17-18th century German community in Jelgava, Latvia. International Journal of
Paleopathology 3: 30–38. DOI: 10.1016/ijpp.2013.01.002.
Pimentel L. 2003. Scurvy: historical review and current diagnostic approach. American
Journal of Emergency Medicine 21: 328-332.
Piontek J. 1977. Średniowieczne Cmentarzysko w Słaboszewie koło Mogilna: analiza
wymieralności. Przegląd Antropologiczny 43: 37–53.
Piontek J. 1981. Biologiczna charakterystyka średniowiecznej populacji wiejskiej ze
Słaboszewa, woj. bydgoskie. In: Źródła do badań biologii i historii populacji słowiańskich,
Malinowski A (ed.). Uniwersytet im. Adama Mickiewicza w Poznaniu, Seria Antropologia
10: 39–83.
Polcyn M. 2003. Archeobotaniczna interpretacja wczesnośredniowiecznych, podwodnych
warstw kulturowych z Ostrowa Lednickiego i Giecza. Biblioteka Studiów Lednickich 9:
Lednica- Poznań.

This article is protected by copyright. All rights reserved.

Porzeziński A. 2006. Wczesnośredniowieczne cmentarzysko szkieletowe na stanowisku 2a w
Cedyni, województwo zachodniopomorskie. Biblioteka Naukowa Muzeum Narodowego w
Szczecinie: Seria Archeologia, Szczecin.
Porzeziński A. 2012. Osadnictwo ziemi cedyńskiej we wczesnym średniowieczu.
Archeologiczne studium osadnicze. Terra Incognita.3: Chojna.
Reitsema LJ, Crews DE, Polcyn M. 2010. Preliminary evidence for medieval Polish diet from
carbon and nitrogen stable isotopes. Journal of Archaeological Science 37: 1413-1423.
Roberts CA, Manchester K. 2005. The archaeology of disease. Third edition. Stroud: Sutton
Publishing Ltd.
Schaefer M, Black S, Scheuer L. 2009. Juvenile osteology, a laboratory and field manual.
Elsevier Academic Press: USA.
Scheuer L, Black S. 2000. Developmental juvenile osteology. Elsevier Academic Press:
Oxford, UK.
Scheuer L, Black S. 2004. The juvenile skeleton. Elsevier Academic Press: Oxford, UK.
Schultz M. 2001. Paleohistopathology of bone: A new approach to the study of ancient
diseases. Yearbook of Physical Anthropology 44: 106–147.
Stone I. 1966. On the genetic etiology of scurvy. Acta Geneticae Medicae et
Gemellologiae 15: 345-350.
Tobolski K. 1991. Wstęp do paleoekologii Lednickiego Parku Krajobrazowego. Biblioteka
Studiów Lednickich: UAM, Poznań.
Tyszkiewicz J. 1983. Dziecko w średniowiecznej Polsce: poczęcie, urodzenie, zdrowie
niemowlęcia. In Wkład starożytności, średniowiecza i renesansu w rozwój nauk medycznych,
Wróblewski W (ed.). Uniwersytet Mikołaja Kopernika, Toruń, pp. 159-170.
Waldron T. 2009. Palaeopathology. Cambridge University Press, Cambridge/NewYork.
Weinstein M, Babyn P, Zlotkin S. 2001. An orange a day keeps the doctor away. Pediatrics
108: e55. DOI: 10.1542/peds.108.3.e55.
White TD, Black MT, Folkens PA. 2012. Human Osteology. Elsevier Academic Press: USA.
Wood JW, Milner GR, Harpending HC, Weiss KM. 1992. The osteological paradox:
problems of inferring prehistoric health from skeletal samples. Current Anthropology 33:
343-370.
World Health Organization (WHO). 1999. Scurvy and its prevention and control in major
emergencies. Geneva: World Health Organization.
Wrzesińska A, Wrzesiński J. 2005. Czytanie z kości. Muzeum Pierwszych Piastów na
Lednicy.
Żołądź-Strzelczyk D. 2002. Dziecko w dawnej Polsce. Wydawnictwo Poznańskie: Poznań.
http://ndb.nal.usda.gov.

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 Table 1. Age-at-death distributions in three examined samples.

Cedynia Ostrów L. 11th- Słaboszewo

Total
Age 10th-14th AD 14th AD 14th-17th AD
categories N % N % N % N %

0-0.5 11 5.5 8 4.1 3 2.7 22 4.3

0.6-2.5 35 17.4 33 17.0 20 18.0 88 17.4

2.6-6.5 56 27.9 64 33.0 26 23.4 146 28.9

6.6-10.5 58 28.8 46 23.7 24 21.6 128 25.3

10.6-14.5 18 9.0 31 16.0 25 22.6 74 14.6

14.6-17.0 23 11.4 12 6.2 13 11.7 48 9.5

Total (0-17) 201 100 194 100 111 100 506 100

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 Table 2. Prevalence of scurvy in examined subadult remains.

Cedynia 10th-14th AD Ostrów Lednicki 11th-14th AD Słaboszewo 14th-17th AD Total

Age
Nt* n Ns** n Nt n Ns n Nt n Ns n Nt n % Ns n %
categories

0-0.5 11 0 5 0 8 0 2 0 3 0 3 0 22 0 0.0 10 0 0.0

0.6-2.5 35 3 18 2 33 2 24 2 20 1 9 1 88 6 6.8 51 5 9.8

2.6-6.5 56 4 26 1 64 0 47 0 26 1 10 0 146 5 3.4 83 1 1.2

6.6-10.5 58 2 37 2 46 2 26 2 24 2 5 1 128 6 4.7 68 5 7.4

10.6-14.5 18 0 17 0 31 1 16 1 25 0 8 0 74 1 1.3 42 1 2.4

14.6-17.0 23 0 10 0 12 0 2 0 13 0 2 0 48 0 0.0 13 0 0.0

Total (0-17) 201 9 (4.5%) 113 5 (4.4%) 194 5 (2.6%) 117 5 (4.3%) 111 4 (3.6%) 37 2 (5.4%) 506 18 3.6 267 12 4.5

*Nt – total sample; **Ns – sample including the skeletons with at least one greater wing of sphenoid

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 Table 3. Skeletal manifestations of scurvy at particular anatomical sites in affected subadults.
Skull Postcranial skeleton

Suggest.
Definite variables Indicative variables Suggestive variables Indicative variables
var.

Sphenoid Scapula Scapula

Maxilla Palate Mandible Zygomatic Zygomatic Infraorbital Cranial Orbital Long bones
Site and Age supras. infras.
gr. wing posterior process coronoid orb. aspect int. aspect foramen vault roof metaphyses
grave no (years) fossa fossa

Cedynia
18 3 – P P – – – – – – – P –
32 9 P – – – – – – A – – – –
65A 1.5 P, H P P, H – – – – P, H P, H P, H – P, H
160A 7 P P P – A P P A P, H – – –
303 6 – – – P – – – – – – P, H –
611 3 – P P P – – – – – – P –
794A 2 – P P P – – – – – – P –
818 4 P – – P – – – P – – P –
968 0.75 P, H – – P, H P P – P P, H P – P

Ostrów L.
707 8 P P P, H P, H A P, H P A P A A A
756 2 P P P, H – – – – – – P P, H P
998 1 P, H P, H P P, H A P – P A P A A
1086 7 P, H – – P, H P P – – – P P, H A
1226 12 P – – P P P – A – P P P

Słaboszewo

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 72 7 P P P – P P P P P – – –
97/15 1 P P P P, H – – P A P – P –
98/16 3 – – – P, H – – – – – P, H P P, H
127/35 7 – – – – – – – – – A P A
Not present for observation (–), abnormal porosity (P), hypertrophic lesion (H), lesions absent (A)

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Fig. 1. Map of Poland with marked locations of three examined sites.

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Fig. 2. Abnormal porosity of the sphenoid bone. A. Ostrów Lednicki 756; B. Cedynia 32; C.
Cedynia 160A; D. Cedynia 968; note a hypertrophic lesion in D.

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Fig. 3. Abnormal porosity and new bone formation of the orbital roof. A. Cedynia 160A; B.
Cedynia 968.

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Fig. 4. Abnormal porosity of the palate. A. Cedynia 794A; B. Ostrów Lednicki 707; C.
Ostrów Lednicki 756; note hypertrophic lesions in B and C.

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Fig. 5. Medial coronoid process of the mandible - abnormal porosity and new bone
formation. A. Ostrów Lednicki 707; B. Ostrów Lednicki 998.

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Fig. 6. Maxilla. A. Ostrów Lednicki 998 - abnormal porosity and new bone formation; B.
Cedynia 794 - abnormal porosity.

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