International Journal of Osteoarchaeology

Int. J. Osteoarchaeol. 18: 178–187 (2008)

Published online 3 July 2007 in Wiley InterScience
(www.interscience.wiley.com) DOI: 10.1002/oa.930

A Likely Case of Scurvy from Early

Bronze Age Britain
S. MAYS*
Ancient Monuments Laboratory, English Heritage Centre for Archaeology, Fort Cumberland,
Eastney, Portsmouth PO4 9LD, UK

ABSTRACT A probable case of scurvy is identified in a child skeleton from England, dating to 2200–1970
BC. Lesions were mainly restricted to the ectocranium, but some endocranial lesions were
also seen. This appears to be the earliest reported example of scurvy from Britain, and adds to
the very few palaeopathological case descriptions available for the disease in infants and
young children from Europe. Copyright ß 2007 John Wiley & Sons, Ltd.

Key words: vitamin C; prehistoric; scorbutic

Introduction about 6 months (Hodges et al., 1971; Stuart-

Scurvy is a disease caused by deficiency of
vitamin C. Humans are unable to synthesise
vitamin C, so it has to be acquired from the diet.
Prime sources of vitamin C are fresh fruit and
vegetables, although it is found to a lesser extent
in other foods such as fish and dairy produce.
Heating or prolonged storage of foods reduces
their vitamin C content. Vitamin C is involved in
the synthesis of collagen, the main structural
protein of the body. Deficiency of vitamin C
leads to a general weakness of connective tissues.
Weakness in blood vessel walls leads to haemor-
rhage, the main lesion in scurvy. Haemorrhage
may, if it occurs adjacent to bone, provoke an
osteological response, which potentially enables
the recognition of scurvy in skeletal remains.
Prolonged deficiency of vitamin C is necessary to
produce disease. Even if there is a total absence of
vitamin C in the diet, the first symptoms
(generally lethargy) do not generally appear
until 1–3 months, and haemorrhages only after
* Correspondence to: Ancient Monuments Laboratory, English
Heritage Centre for Archaeology, Fort Cumberland, Eastney, Ports-
mouth PO4 9LD, UK.
e-mail: simon.mays@english-heritage.org.uk
Copyright # 2007 John Wiley & Sons, Ltd.
Macadam, 1989; Beck, 1997; Aufderheide &
Rodrı́guez-Martı́n, 1998: 310; Ortner, 2003:
383–4; Pimentel, 2003).
The current work is a case report of a possible
prehistoric example of scurvy from England. This
publication was prompted by the observation that
scurvy has rarely been identified in British
remains and that the case appears to be the
earliest yet known from Britain.
Materials and methods
Excavations at a Bronze Age round barrow at
Barrow Clump, Wiltshire, England, were under-
taken as part of a research project to study badger
damage to ancient barrows (Last, unpublished),
and yielded 14 inhumations. One of these, burial
6010, a child, showed possible signs of scurvy and
is the subject of the present work. Burial 6010 was
a flexed inhumation sealed beneath the barrow
mound (Figure 1). The grave was lined with flint
nodules, and a bell-beaker was found near the feet
of the burial. Radiocarbon determination
(OxA-16643) indicates a calibrated date range
(95% confidence limits) of 2200–1970 BC.
Received 8 January 2007
Revised 16 March 2007
Accepted 30 March 2007
Bronze Age Scurvy
Figure 1. The Bronze Age burial under excavation. This figure is available in colour online at www.interscience.
wiley.com/journal/oa.
Skeletal survival is depicted in Figure 2. The
skull is fairly complete and shows minimal
post-depositional erosion (generally 0–1 on the
scale of McKinley, 2004), although there is some
damage to facial elements. The post-cranial
skeleton, by contrast, survives poorly; preserved
elements consist mainly of long-bone shaft
fragments, and the degree of surface erosion
varies from 0–5 on the scale of McKinley (2004).
Dental development (Gustafson & Koch, 1974)
indicates an age at death of about 2 years. No
attempt was made to determine sex. The skeleton
was examined for abnormalities, and any which
were apparent were evaluated both grossly and
using a low-power binocular microscope. Because
of the fragmented nature of the remains, no
radiographic examination was attempted.
Results
The skull displayed abnormalities consisting
principally of porosity of bone surfaces and new
bone deposits. On the external surface of the cranial
vault there is abnormal porosity in the glabella
area and on the right temporal bone. The external
surface of the right greater wing of the sphenoid
Copyright # 2007 John Wiley & Sons, Ltd.
179
is somewhat porous (Figure 3a) (the left is too
damaged to permit assessment). Changes to the
sphenoid bone are subtle, but comparison with a
series of sphenoids from normal individuals of
about the same age at death seems to confirm that
the sphenoid from this burial is abnormal. Pores
in the cortex of normal sphenoid bones tend to be
few in number, fairly large, and often enter the
cortex at an oblique angle (Figure 3b). By
contrast, those in the Barrow Clump specimen
are finer, greater in number, and tend to enter the
bone at more vertical angles (Figure 3a).
There are thick deposits of porous new bone
on the orbital roofs (Figure 4). The deposits have
small channels which indicate the courses of
minor blood vessels. There is no indication of
diploic hyperplasia. The inferior and lateral walls
of the right orbit show abnormal porosity
(Figure 5) (the corresponding areas of the left
orbit are missing). There is abnormal porosity of
the posterior surface and zygomatic process of
the right maxilla. The inferior surface of the hard
palate shows increased porosity (Figure 6). There
is abnormal porosity of the medial surfaces of the
coronoid processes of the mandible (Figure 7).
On the endocranial surface there is new bone
deposition in the region of the internal occipital
Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
180
Figure 2. Schematic depiction of skeletal elements pre-
sent.
protuberance and on the right side of the
sphenoid bone on the greater and lesser wings.
There is porosis of the internal surface of the right
greater wing of the sphenoid and right temporal
squama (the antimeres of these elements are too
damaged to permit assessment). There are two
discrete areas of ‘branched lysis’ – multiple
contiguous small channels in the bone surface
– on the internal surface of the right parietal bone
(Figure 8). These areas of branched lysis connect
to channels whose morphology indicates that
they conveyed blood vessels. A similar area of
branched lysis is present on the endocranial
surface of the occipital bone.
Copyright # 2007 John Wiley & Sons, Ltd.
S. Mays
The anterior fontanelle is open and unusually
large for a child of this age. It measures
approximately 6cm (transversely) by 3 cm (ante-
ro-posterior). More than 95% of anterior
fontanelles close by 2 years (Aisenson, 1950),
and the persistence of one of this size is clearly
abnormal (Lyall et al., 1991). The posterior
fontanelle presents a normal, fully closed appear-
ance.
In the post-cranial skeleton, the only evidence
for abnormality is a deposit of woven bone on the
medial surface of the shaft of the left tibia.
Diagnosis
In a series of studies (Ortner & Eriksen, 1997;
Ortner et al., 1999, 2001; Ortner, 2003) Ortner
and his associates described, taking into account
clinical evidence and anatomical relationships
between bone and overlying blood vessels and
other soft tissue structures, a constellation of
pathological changes in the cranial and post-
cranial skeleton of infants and young children
which, they argued, are indicative of scurvy.
When haemorrhage occurs adjacent to bone it
may stimulate the periosteum to produce new
bone. It may also provoke a localised inflamma-
tory response, the vascular component of which
may result in the proliferation of capillaries in the
affected area. This may result in locally increased
bone porosity to provide pathways for these
blood vessels through bone. The changes
described by Ortner and colleagues thus consist
of abnormal bony porosity and deposition of new
bone upon existing cortex. Typical locations for
lesions are on the external surface of the skull;
sites specifically affected include the superior,
lateral and inferior orbital walls, the greater wing
of the sphenoid, the posterior surface of the
maxilla, the medial surface of the zygomatic
bone, and the medial surface of the coronoid
process of the mandible. The orbital lesions may
relate to haemorrhage caused by eye movement;
the others may relate to haemorrhage caused by
muscular movements involved in chewing: the
temporalis muscle passes between the greater
wing of the sphenoid and the zygomatic bone
and inserts on the medial surface of the coronoid
process of the mandible. Lesions are often seen on
Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
Bronze Age Scurvy 181

Figure 3. (a) Right greater wing of the sphenoid, showing abnormal porosity. (b) Right greater wing of the sphenoid from
a normal two-year-old child for comparison; although there are some pores in the cortex, they are fewer and larger than
in the Barrow Clump specimen and tend to enter the bone at oblique angles. This figure is available in colour online at
www.interscience.wiley.com/journal/oa.

Figure 4. Roof of right orbit, showing thick deposits of porous bone. This figure is available in colour online at
www.interscience.wiley.com/journal/oa.

Copyright # 2007 John Wiley & Sons, Ltd. Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
182 S. Mays

Figure 5. Inferior wall of right orbit showing abnormal porosity. This figure is available in colour online at www.
interscience.wiley.com/journal/oa.

Figure 6. The inferior surface of the hard palate of the Barrow Clump individual (at left in photograph) shows abnormal
porosity. The specimen at right is from a normal two-year-old child for comparison. This figure is available in colour online
at www.interscience.wiley.com/journal/oa.

Copyright # 2007 John Wiley & Sons, Ltd. Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
Bronze Age Scurvy 183

Figure 7. The medial surface of the left mandibular ramus of the Barrow Clump burial (at left in photograph) shows
abnormal porosity at the base of the coronoid process. The specimen at right is from a normal two-year-old child for
comparison. This figure is available in colour online at www.interscience.wiley.com/journal/oa.

the inferior surfaces of the palatine processes of scurvy in the cranial bones are on the ectocranial
the maxillae; haemorrhage due to minor traumata surface of the skull vault and around the
during feeding and mastication may account for infra-orbital foramen on the maxilla. In the
these. Other characteristic locations for lesions of post-cranial skeleton, the infra- and supra-spinous

Figure 8. Internal view of part of the right parietal bone showing presence of multiple contiguous bony channels
(‘branched lysis’). Note that the area of branched lysis connects with channels whose morphology clearly indicates they
conveyed blood-vessels (toward the top right of the photograph). This figure is available in colour online at www.
interscience.wiley.com/journal/oa.

Copyright # 2007 John Wiley & Sons, Ltd. Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
184
fossae of the scapulae and the metaphyses of long
bones are favoured sites for lesions.
The current case shows periosteal new bone
formation or porosis in most of the cranio-
mandibular sites identified by Ortner and
colleagues (Ortner & Eriksen, 1997; Ortner
et al., 1999, 2001; Ortner, 2003) as typical of
scurvy. Evaluation of the post-cranial skeleton
was inhibited by poor survival of elements other
than long-bone shaft fragments – for example,
neither scapula was present and only a few
fragments of metaphysial parts of long bones
were preserved. Although none of the individual
changes seen in the current case is on its own
diagnostic, taken together they are strongly
indicative of scurvy, and no other conditions
can realistically be considered differential diag-
noses.
It seems reasonable to suppose that the porosis
and new bone deposition seen endocranially in
the current case are indicative of intra-cranial
haemorrhage. The areas of branched lysis also
appear to be connected with haemorrhage; their
morphology is suggestive of bony resorption due
to proliferation of small blood vessels on the
endocranial surface and they connect with
morphologically normal blood vessel channels.
Subdural haemorrhage is well documented in
clinical cases of scurvy (Miura et al., 1982;
Clemetson, 2003), so it seems likely that these
endocranial lesions are due to scurvy in this case.
Turning to the open anterior fonanelle, a
variety of conditions, including rickets, hydro-
cephalus, hypothyroidism and cleidocranial dys-
ostosis, may delay closure of the fontanelle
(Aisenson, 1950), but there is no evidence of
these conditions in the current material. The
cause of the persistence of the anterior fontanelle
is unclear, but there is no reason to suppose that it
is connected with vitamin C deficiency.
Discussion
Few cases of scurvy have been identified in British
remains. The only prehistoric case from Britain
reported in the literature appears to date from the
1st century BC (Roberts & Manchester, 1995:
172–3), although earlier cases (Neolithic) have
been reported from central Europe (Carli-Thiele,
Copyright # 2007 John Wiley & Sons, Ltd.
S. Mays
1996). Published descriptions of scurvy from the
historic periods in Britain are sparse. References
to a few possible cases are made in some general
palaeopathological surveys (Lewis, 2002; Roberts
& Cox, 2003). Six cases have recently been
identified in a group of 19th century AD skeletons
(Brickley & Ives, 2006). There are several possible
explanations for the dearth of reported cases of
scurvy.
Firstly, there may be a problem of under-
diagnosis. In adults, lesions of scurvy tend to be
rather minor, making it difficult to identify
(Ortner, 2003). Although lesions in infants and
young children are more pronounced, it is only
recently (Ortner & Eriksen, 1997) that the
changes of infantile scurvy have been adequately
collated for palaeopathologists. Prior to this,
there may, for example, have been a tendency to
consider porous lesions of the skull vault and
orbital roofs as indicative of anaemia without
adequate consideration of differential diagnoses
such as scurvy.
Secondly, given that palaeopathological
recognition of scurvy is largely dependent upon
its identification in infant and young child
remains, biases in the skeletal record may be
relevant. During many periods, the infant/young
child cohort is under-represented in British
archaeological material. It is likely that this
reflects mainly differential burial practices, with
frequent disposal of young individuals in ways
which have not left archaeological traces. It may
also reflect poorer survival in the soil of the fragile
bones of infants and young children.
Thirdly, scurvy may have been a genuinely rare
condition in early Britain. Documentary sources
for the historic period show that, prior to the
Industrial Revolution, when diets were deficient it
tended to be in protein rather than in fruit and
vegetables (Gies & Gies, 1990). Infantile scurvy
first began to be noted as a regular problem only
from about the 1870AD when wealthier social
classes began to feed their infants on bread and
milk sterilised by heating (which destroys the
vitamin C). Prior to this it does not appear to have
been a widespread disease in infants (although a
few cases were reported in the 16th and 17th
centuries), perhaps because prolonged breast-
feeding and weaning using vegetable-based foods
had a protective effect (Mays, in press). The
Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
Bronze Age Scurvy
presence of scuvy in the Barrow Clump child
suggests that breastfeeding must have ceased
some time before death as this would have
provided it with vitamin C. Whether this was
normal practice or whether the child had suckling
difficulties is unclear. Perhaps food given to the
child was heated to such an extent to destroy any
vitamin C content.
The few systematic archaeological surveys that
have been carried out investigating scurvy in
juvenile skeletal remains from early Britain tend to
bear out the suggestion that scurvy was rare.
Melikian & Waldron (2003) examined 123
subadult skeletons from the historic period in
Britain for porosity. Virtually all skulls were found
to show porosity in one or more areas, but the
authors indicate that they felt no case was
suggestive of infantile scurvy. Much of the
porosity they observed may have been normal
skeletal morphology or due to diseases other than
scurvy. A systematic evaluation of juvenile
skeletal remains has been carried out on skeletal
material from medieval Wharram Percy (Connell
& Mays, unpublished). Remains were evaluated
using the diagnostic criteria of Ortner & Eriksen
(1997). Care was also taken to distinguish
abnormal from normal porosis and to distinguish
porous lesions of scurvy from those of different
causes such as anaemia or rickets. The most
important location for lesions in scurvy appears to
be the greater wing of the sphenoid bone (Ortner
& Eriksen, 1997), so Connell & Mays (unpub-
lished) included in their study only those
individuals with one or both greater wings of
sphenoid preserved. Of the 183 satisfying this
condition, none showed scurvy. Nor was there
any sign of it in a further 76 juveniles from
Wharram Percy where greater wings of sphenoid
were missing but which preserved other cranial
bones.
Conclusions
The current case shows porosis or new bone
formation at most of the locations in the skull
identified by Ortner and colleagues (Ortner &
Eriksen, 1997; Ortner et al., 1999, 2001; Ortner,
2003) as characteristic of scurvy. However, the
Copyright # 2007 John Wiley & Sons, Ltd.
185
poor survival of post-cranial parts means that
evidence for scurvy in these elements could not
be adequately assessed. For this reason, this case
is presented merely as a likely case of scurvy,
although it must be said that it is difficult to think
of another diagnostic option that can plausibly
account for the lesions. Endocranial features of
new bone formation, porosis and branched lysis
were seen in the current case. It was argued that
they may be due to intra-cranial haemorrhage,
which is seen clinically in scurvy, and hence that
they are a manifestation of scurvy rather than
simply a coincidental finding. The palaeopatho-
logical interpretation of endocranial lesions of
this type is controversial, and it is likely that more
than one cause may lead to their formation
(Lewis, 2004). It is suggested here that scurvy
may be one cause of such lesions. Although
endocranial new bone formation, porosis or
branched lysis are not in themselves pathogno-
monic of scurvy, when present with other lesions
suggestive of scurvy they serve to strengthen that
diagnosis. It is suggested that these endocranial
lesions be evaluated, in addition to the features
identified by Ortner and co-workers (Ortner &
Eriksen, 1997; Ortner et al., 1999, 2001; Ortner,
2003), when surveying skeletal collections for
scurvy.
It is important to distinguish scurvy from other
potential causes of bony porosity. This is
particularly pertinent for orbital roof porosity
which may have a variety of other causes, most
notably rickets and anaemia. However, careful
examination may enable different options to be
distinguished. For example, orbital lesions in
scurvy would be expected to consist of new bone
deposited upon an underlying normal cortical
surface, or else small pores in the otherwise
normal cortical surface. There is no marrow
hyperplasia (Ortner et al., 2001: Ortner, 2003:
388–9). In rickets, bone surfaces may be rather
spicular, and superficial pores are rather larger
and, in contrast to scurvy, represent voids as a
result of imperfect mineralisation of the growing
surface – these holes would have been filled with
unmineralised osteoid in life rather than transmit-
ting blood vessels (Ortner & Mays, 1998). In
anaemia, the surface porosity is a result of marrow
hyperplasia, visible in broken cross-sections or
radiographically (Ortner, 2003: 370f). Careful
Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
186
evaluation of morphology of lesions, and of the
distribution of pathological changes in the skull
and post-cranial skeleton, often help to advance
one diagnosis at the expense of others. However,
a firm diagnosis of cranial porosity may not
always be possible, and it should also be recalled
that more than one condition may be present in
the same individual.
The current case is a rare report of scurvy in an
early British skeleton. Although under-diagnosis
and biases in the skeletal record may play a part in
the rarity with which scurvy has been reported in
British material, the case was made that it may
genuinely have been a rare disease prior to the
late post-medieval period. However, careful,
systematic analysis of British juvenile skeletons,
with care taken not only to distinguish abnormal
from normal porosity, but also in differentiating
different causes of porosis, would be required to
confirm or refute this suggestion.
Acknowledgements
Thanks are due to Jonathan Last, English Heri-
tage Centre for Archaeology, for supplying back-
ground information on Barrow Clump.
References
Aisenson MR. 1950. Closing of the anterior fontanelle.
Pediatrics 6: 223–226.
Aufderheide AC, Rodrı́guez-Martı́n C. 1998. The Cam-
bridge Encyclopaedia of Human Palaeopathology. Cam-
bridge University Press: Cambridge.
Beck SV. 1997. Scurvy: citrus and sailors. In Plague, Pox
and Pestilence: Disease in History, Kiple KF (ed.).
Weidenfeld & Nicholson: London; 68–73.
Brickley M, Ives R. 2006. Skeletal manifestations of
infantile scurvy. American Journal of Physical Anthro-
pology 129: 163–172.
Carli-Thiele P. 1996. Spuren von Mangelerkrankungen an
steinzeitlichen Kinderskeleten, Fortschritte in der Paläo-
pathologie und Osteoarchäologie; Bd. 1. Erich
Goltze: Göttingen.
Clemetson CAB. 2003. Child abuse or Barlow’s dis-
ease? Pediatrics International 45: 758.
Connell B, Mays S. Unpublished. Scurvy Among The
Juvenile Skeletal Remains From Wharram Percy. Manu-
Copyright # 2007 John Wiley & Sons, Ltd.
S. Mays
script compiled 1997, held on file at English Heri-
tage, Portsmouth.
Gies F, Gies J. 1990. Life in a Mediaeval Village. Harper &
Row: London.
Gustafson G, Koch G. 1974. Age estimation up to 16
years of age based on dental development. Odonto-
logisk Revy 25: 297–306.
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.
Last J. Unpublished. Badger-Damaged Round Barrows
Near Stonehenge and Avebury. Manuscript compiled
2003, held on file at English Heritage, Portsmouth.
Lewis M. 2002. Urbanisation and Child Health in Medieval
and Post-Medieval England. BAR British Series 339.
Archaeopress: Oxford.
Lewis ME. 2004. Endocranial lesions in non-adult
skeletons: understanding their aetiology. Inter-
national Journal of Osteoarchaeology 14: 82–97.
Lyall H, Ogston SA, Paterson CR. 1991. Anterior
fontanelle size in Scottish infants. Scottish Medical
Journal 36: 20–22.
Mays S. In press. Metabolic disease. In Advances in
Human Palaeopathology, Pinhasi R, Mays S (eds).
Wiley: Chichester.
McKinley JI. 2004. Compiling a skeletal inventory:
disarticulated and co-mingled remains. In Guidelines
to the Standards for Recording Human Remains, Brickley
M, McKinley JI (eds). British Association for Bio-
logical Anthropology and Osteoarchaeology/Insti-
tute of Field Archaeology: Southampton/Reading;
14–17.
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.
Miura T, Tanaka H, Yoshinari M, Tokunaga A, Koto
S, Saito K, Izumi J, Inagaki M. 1982. A case of
scurvy with subdural haematoma. Rinsho Ketsueki 23:
1235–1240.
Ortner DJ. 2003. Identification of Pathological Conditions in
Human Skeletal Remains (2nd edn). Academic Press:
London.
Ortner DJ, Eriksen 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, Mays S. 1998. Dry-bone manifestations of
rickets in infancy and early childhood. International
Journal of Osteoarchaeology 8: 45–55.
Ortner DJ, Kimmerle EH, Diez M. 1999. Probable
evidence of scurvy in subadults from archaeological
Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa
Bronze Age Scurvy
sites in Peru. American Journal of Physical Anthropology
108: 321–331.
Ortner DJ, Butler W, Cafarella J, Milligan L. 2001.
Evidence of probable scurvy in subadults from
archaeological sites in North America. American
Journal of Physical Anthropology 114: 343–351.
Pimentel L. 2003. Scurvy: historical review and cur-
rent diagnostic approach. American Journal of Emer-
gency Medicine 21: 328–332.
Copyright # 2007 John Wiley & Sons, Ltd.
187
Roberts C, Cox M. 2003. Health and Disease in Britain.
Sutton: Stroud.
Roberts C, Manchester K. 1995. The Archaeology of
Disease (2nd edn). Sutton: Stroud.
Stuart-Macadam P. 1989. Nutritional deficiency dis-
ease: a survey of scurvy, rickets and iron deficiency
anaemia. In Reconstruction of Life From the Skeleton, Işcan
MY, Kennedy KAR (eds). Alan Liss: New York;
201–222.
Int. J. Osteoarchaeol. 18: 178–187 (2008)
DOI: 10.1002/oa