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Article history:
Received 3 September 2012
Received in revised form 5 September 2013
Accepted 5 September 2013
Keywords:
Vitamin C deciency
Rickets
Differential diagnosis
Eten
a b s t r a c t
Scurvy is a disease caused by vitamin C deciency and is a key paleopathological indicator of subadult
health and nutritional status in the past. Yet, little is known about scurvy in human remains from South
America and the Peruvian Central Andes in particular. In the Lambayeque Valley Complex on the north
coast of Peru, a sample of 641 archaeologically recovered subadults (A.D. 9001750) were scored for the
skeletal manifestations of vitamin C deciency, testing the hypotheses that scurvy was common in this
region and that prevalence increased following European contact. The ndings reveal only ve convincing cases of scurvy; overall prevalence appears extremely low, and scurvy did not become perceptibly
more common following conquest. Of diagnostic interest, complex ectocranial vascular impressions were
documented in two cases. Though rarely attributed to scurvy, examination suggests they formed during
scorbutic episodes. Another Colonial Period subadult may demonstrate comorbidity between scurvy and
rickets. This work also provides new questions for the investigation of scurvy in Andean South America.
2013 Published by Elsevier Inc.
1. Introduction
Scurvy is a metabolic disorder produced by chronic inadequate
intake of vitamin C. As one of the central goals of paleopathology
and bioarchaeology is to reconstruct health and nutrition in the
past, scurvy ranks as a key variable in the assessment of nutritional stress and dietary adequacy in human populations. While
scurvy has long been underreported in the paleopathological literature, it has received increasing perception, focus, and diagnostic
rigor, particularly over the last decade. This visibility is largely
due to the development of Donald Ortners diagnostic criteria of
scurvy in the skull (Ortner and Eriksen, 1997; Ortner et al., 1999,
2001) and postcranial skeleton (Ortner, 2003). Subsequent studies
have shed new light on dietary insufciency, subsistence economy, humanecology synergisms, urbanism, and socioeconomic
inequality (e.g., Melikian and Waldron, 2003; Lewis, 2004; Brickley
and Ives, 2006, 2008; Mays, 2008; Waldron, 2009; Lewis, 2010;
van der Merwe et al., 2010a,b; Brown and Ortner, 2011; Geber and
Murphy, 2012).
Table 1
Diagnostic criteria for scurvy used in this study, drawn from Ortner (2003), Ortner
et al. (1999), and Brickley and Ives (2008).
Anatomical site
Criteria
Cranial vault
Temporal bone
Zygomatic bone, internal
and external surfaces
Anterior maxilla
Infraorbital foramen
Hard palate
Coronoid process of the
mandible, medial surface
Long bone diaphyses
Long bone metaphyses
Supra- and infraspinous
fossa of the scapula
Ribs
35
36
37
Fig. 1. The Lambayeque Valley Complex on the north coast of Peru, showing the location of key archaeological sites including Chornancap (1), Jotoro (2), and Eten (3) where
cases of subadult scurvy have been identied.
+
+
Fig. 3. Anterior view of the skull, Case 1. Areas of abnormal porosity, along with
vascular impressions and patches of ne bone deposition, were observed superior
to glabella, on the left and right nasal bones, and in midfacial region.
Key: +, present; , absent; and n/o, not observable.
+
+
+
n/o
Case 1 (57 years old)
Case 2 (1621 months old)
Case 3 (4.55.5 years old)
Case 4 (1621 months old)
Case 5 (11.5 years old)
+
+
+
+
+
+
+
+
+
n/o
+
+
n/o
n/o
Long Bone
metaphyses:
fracture,
cortical
thinning, new
bone
formation
Long bone
diaphyses:
new bone
formation
Supra- and
infraspinous
fossa of the
scapula:
abnormal
porosity, new
bone
formation
Coronoid
process of the
mandible: new
bone formation
Infraorbtial
foramen, hard
palate: new
bone formation
Anterior and
posterior
zygomatic
bone:
abnormal
porosity, new
bone
formation,
vascular
impressions
Anterior and
posterior
maxilla:
abnormal
porosity, new
bone
formation,
vascular
impressions
Temporal
bone:
abnormal
porosity
Superior eye
orbits:
abnormal
porosity, new
bone formation
Greater wing
of the
sphenoid
bone:
abnormal
porosity
Cranial vault:
abnormal
porosity, new
bone
formation,
vascular
impressions
Table 2
Distribution of pathological loci, Cases 15.
Ribs: fractures
adjacent to
oestochondral
junction;
aring rib ends
38
39
Fig. 4. Vascular impressions on the ectocranial surface of the frontal bone of Case 1.
These appear to be bony impressions of abnormal and tortuous vascular networks,
the two largest of appear to have anastomosed.
new bone (Fig. 6a). While both orbits were affected, the degree of
porosity was asymmetrical and affected the left orbit in a more pronounced fashion than the right. Extensive and widespread deposits
of new bone covered much of this childs left and right anterior
maxillae, particularly at the attachment sites of the Quadratus labii
superioris, Caninus, Transverse nasalis, and Incisive muscles (Fig. 6b).
The left and right posterior maxillae featured very porous new
bone and bilateral blood vessel tracking within new bone deposits
(Fig. 6c). The right ascending ramus of the mandible showed evidence of minor inammation in areas associated with the insertion
of the Temporalis muscle, but this was not bilateral. Mild abnormal
porosity was also noted at the mental eminence of the mandible
near the origins of the Mentalis and Orbicularis oris muscles. No
postcranial abnormalities were present.
Fig. 6. In Case 2, abnormal porosity and new bone formation was present on the
left and right orbital plates (A) and the left and right anterior (B) and posterior (C)
maxillae.
In Case 4, abnormal porosity and hypertrophic new bone formation was observed in the eye orbits, posterior maxillae, and both
greater wings of the sphenoid bone (Fig. 8). Patches of ne new
bone formation were also observed on the endocranial surfaces of
the fontal bone. Upper limb bones were also affected (Fig. 9). The
posterior diaphysis of the right humerus was covered in a very ne
but irregular distribution of woven bone. Anteriorly, the superior
humeral metaphysis was characterized by ragged surfaces. Similar features were present on the metaphyses of both ulnae and
radii, qualitatively resembling a slit/strut morphology (Ortner
In Case 3, abnormal porosity was observed on the right temporal bone at the posterior root of the zygomatic arch along and
inferior to the attachment of the Temporalis m. Porosity of the
orbital roofs was noted, associated with irregular areas of wellorganized, smooth compact bone overlying the cortex, consistent
with a well-organized hematoma (Fig. 7A). Both left and right
posterior maxillae exhibit abnormal porosity and supercial vessel tracking. The superior and lateral aspects of the frontal bones
ectocranial surface was covered with remnants of multiple vascular ramus-like blood vessel impressions (Fig. 7B) and included
one prominent channel system extending into a raised region of
well-healed porosity. Both parietal bosses were characterized by
roughly circular, elevated, and bilateral porotic loci ringed by tortuous vascular impressions (Fig. 7C). These loci are in line with the
morphology and location of Parrotts swellings (Brickley and Ives,
2008). No postcranial abnormalities were observed.
4.4. Case 4: CNS Burial U4AE-2 (1621 months old)
40
Fig. 9. Abnormalities of upper limb bones were affected in Case 4, and included
bone formation on the posterior diaphysis and a porous olecranon fossa of the
right humerus. Metaphyses and diaphyses of left and right radii and ulnae also
demonstrated atypical porosity and new bone formation.
Fig. 7. The cranium of Case 3 was characterized by: (A) abnormal porosity and wellorganized new bone on the orbital roofs; (B) complex blood vessel impressions
on the frontal bone, and (C) elevated and bilateral porotic loci ringed by tortuous
vascular impressions on the left and right parietal bosses.
Fig. 8. Multiple sites of the cranium in Case 4 exhibited abnormal porosity and bone
formation, including the superior eye orbits.
and Mays, 1998). The surface of the right olecranon fossa was
notably porous. This may be explained as a vascular response to
the presence of hemarthrosis. On the radii, pathological new bone
was present in the regions overlaid by the Flexor pollicis longus and
Pronator quadratus muscles. Also, the distal radial epiphyses were
cupped. On the ulnae, abnormal bone formation was present in
regions involved with the Abductor pollicis longus origin and the
Brachialis insertion.
4.5. Case 5: CNS Burial U3-91 (11.5 years old)
Case 5 presented abnormal porosity on sphenoid bone fragments, posterior maxillae, and on both superior orbital plates.
Cranial vault fragments displayed ne porosity. In this example,
inammatory response and new bone formation was present on the
endocranial surfaces of the frontal, temporal and occipital bones.
The frontal bone lesions featured very ne vascular impressions or
capillary lesions (Lewis, 2004) involving new bone organization
and formed around vasculature (Fig. 10).
On the postcranial remains of Case 5, porosity and new bone
was observed on the oor of the supraspinous fossa of the right
scapula (Fig. 11A). The diaphysis of the right ulna possessed areas
of ne and coarse porosity in a shell-like layer of pathological bone
that abnormally thickened most of the shaft (Fig. 11B). This was
most pronounced around the areas overlain by the Abductor pollicis
longus, Extensor pollicis longus, and Extensor indicis muscles.
Both femora and tibiae exhibited pronounced bilateral diaphyseal thickening due to massive pathological new bone deposition
(Figs. 12 and 13A). The margins demarcating ber bone formation from normal cortical surfaces were very sharply dened in
terms of texture and coloration, and the anterior tibial crests were
41
Fig. 10. The endocranial surfaces of the frontal bone in Case 5 were marked by new
bone formation associated with an inammatory response.
Fig. 12. Anterior view of the left and right femora and tibiae of Case 5, demonstrating
abnormal new bone formation and signicant diaphyseal thickening of the tibiae.
Fig. 11. Abnormal porosity and new bone formation affected the oor of the
supraspinous process of the right scapula (A) in Case 5, in addition to areas of
ne and coarse porosity associated with a shell-like layer of pathological bone that
abnormally thickened most of the diaphysis of the right ulna (B).
Fig. 13. Detail views of regions of new bone formation on the tibiae of Case 5.
Extremely ne deposits of new bone (A) suggest an active condition at the time
of death, and in some areas, the leading edge of bone formation possessed very ne
(literally, razor-thin) but clearly denable margins of newly mineralized bone (B,
arrow) overhanging healthy cortical surfaces.
42
meningitis, rickets, and scurvy. Further elaboration of these differential diagnoses is supplied in the online Supplementary Materials
that accompany this article.
Some cranial lesions, such as the anterior and posterior maxillae of Cases 1, 3, 4, and 5, and postcranial lesions in Cases 4
and 5, could reect the presence of chronic infectious processes.
Chronic infectious processes producing periosteal inammation
and pathological new bone formation (Larsen, 1997; Ortner, 2003)
may produce plaque-like, sclerotic, and elevated bone deposits.
Under such conditions, new bone can form on any osseous surface but commonly predilects tibial diaphyses bilaterally, such as
Case 5. Such responses due to infection are often more supercial,
patchy, and localized, not producing circumferential modication
of affected bone. Non-specied infection is also a poor explanation
for new bone formation observed on various anterior and posterior maxillae or long bones in Cases 4 and 5, especially since these
lesions are closely associated with muscle attachments and actions.
A differential diagnosis of congenital or acquired treponemal disease in Cases 4 and 5 can be rejected due to the lack of focused
bone apposition on the anterior tibiae (i.e., the sabre-shin deformity absence of caries sicca, and the absence of associated dental
stigmata.
Chronic anemias produced by hemoglobinopathies, hemolyises,
or vitamin deciencies can produce porotic lesions of the cranial vault via hypertrophy of the diplo and may closely resemble
scurvy. However, with every vault lesion reported here in Cases
15, it is possible to rule out marrow hypertrophy fairly easily.
Marrow hypertrophy and enlargement of the diplo occurs at the
expense of the outer table; in these crania, porosity penetrates an
intact outer table. Also, the greater wing of the sphenoid bone is
unlikely to become porous under anemic conditions because it contains minimal marrow space. The oval osseous prominence in Case
1 and the formation of bone atop the anatomical surface of eye
orbits in Cases 3 and 4 are defects that overlay the external lamina, consistent with an organized hematoma. They do not represent
enlarged marrow spaces.
Specic bone-forming disorders may also resemble scorbutic
changes. Hypertrophic (pulmonary) osteoarthropathy (or HO; also
known as Marie-Bamberger Syndrome) is a condition potentially
responsible for new postcranial bone formation in Cases 4 and 5. A
neurocirculatory mechanism associated with forms of pulmonary
inammation and cancers likely stimulates osteoblasts to produce pathological bone (Aufderheide and Rodrguez-Martin, 1998;
Resnik, 2002; Ortner, 2003). However, the onset of this syndrome
typically occurs during adolescence or yet later in life. Children
are rarely affected by the disorder. Cases 4 and 5 also lack the
expected dense candle wax formation on long bone diaphysis and
digital clubbing of hands and feet often associated with HO. Hypertrophic osteoarthropathy cannot account for the cranial lesions
since it typically spares the skull, and only may affect the inner table
(Aufderheide and Rodrguez-Martin, 1998, 91). HO spares muscle
attachment sites (Ortner, 2003, 354), in contrast to locations of
postcranial new bone formation seen in Cases 4 and 5.
Infantile cortical hyperostosis, or Caffeys disease, could t
many lesion descriptions here, as it involves long bone and cranial periosteal inammation and cortical thickening (Caffey, 1946;
Herring, 2007). Demographically, infantile cortical hyperostosis
is unlikely in all cases since it actively manifests in children
mostly between 0 and 6 months of age. The lesions further do
not match those associated with the persistent disease variant in
older children (Resnick, 2002). Infantile cortical hyperostosis disease also tends to produce asymmetrical and unilateral lesions of
the mandible, ribs, and metatarsals, none of which were present.
Endocranial lesions seen in Cases 4 and 5 could be a product
of inammatory meningitis that involves intracranial hemorrhage
(Nelson, 2006). Meningitis can form lesions through a similar
pathophysiological process and produce identical lesion morphology to those observed in Cases 4 and 5. While the presence of
multiple additional cranial and postcranial features all point to
scurvy in these two skeletons, comorbidity with inammatory
meningitis cannot be ruled out without a histological diagnosis
(e.g., Schultz, 2001; Walper et al., 2004).
Metabolic disorders, such as rickets, may produce near-identical
lesions to scurvy, but subtle distinguishing characteristics can help
discriminate between vitamin C and vitamin D deciency (Ortner
and Mays, 1998; Ortner, 2003; Brickley and Ives, 2008). Rachitic
cranial lesions tend toward ultra-ne deposits of porous periosteal
bone, and are often far ner than those recorded in Cases 1 thru
5. In all but Case 4, there is an absence of abnormal curvature of
long bones or other elements associated with weight bearing on
bones possessing inadequate mechanical strength. Other pathological morphologies associated with rickets, including thickened
rib diaphysis, rib attening at the costochondral junction (rachitic
rosary), and pelvic deformation was absent.
Scurvy represents the remaining differential diagnosis. The
specic constellations of lesions appear most consistent with a
diagnosis of scurvy in each case, including abnormal porosity of the
greater wing of the sphenoid bone in Cases 1, 2, 4, and 5 (lesions
considered by the Ortner criteria to be virtually pathognomonic
for scurvy), additional cranial and maxillary sites, and new bone
formation associated with the location and movement of various
muscles associated with mastication and movement of limbs. No
other known pathological condition of the skeleton is known to produce similar bony changes. Though the greater wing of the sphenoid
bone was not affected in Case 3, the combination of other lesions
in this childs remains is most consistent with mechanisms involving pathological inammation and subsequent new bone formation
associated with scorbutic hemorrhage.
However, in Case 4, co-morbidity between scurvy and rickets
should be considered. In addition to the apparent scorbutic lesions,
there was minor yet perceptible deection of the distal radius and
medial bowing of the ulnae and radial epiphyseal cupping. For
a child of this age, it may reect weight bearing on the upper
limbs associated with the locomotion of pushing up and crawling before walking commenced. Further, the morphology of the
affected upper limb long bone metaphyses in Case 4 bear strong
qualitative resemblance to the slit/strut morphology associated
with the metaphyseal ends of rachitic long bones (Ortner and Mays,
1998, Fig. 4). These formations represent parallel zones of alternatingly mineralized and unmineralized osteoid. These features
maximize biomechanical strength under adverse metabolic conditions. The struts provide greater resistance to bending and provide
a basis for rapid and full mineralization once vitamin D becomes
available again (Ortner and Mays, 1998, 53).
5.2. Scurvy in Lambayeque: rst assessment and questions for
future research
Both research hypotheses are rejected. The current data indicate
scurvy in Lambayeque was a rare disease condition, and prevalence did not evidently increase during the postcontact era. An
overall crude prevalence rate is currently calculated as 0.79% (or
5/641 subadults) for the combined late pre-Hispanic and Colonial eras. This stands in clear contrast to a crude prevalence rate
of 10.5% in the NMNH collection drawn from the Peruvian central coast and highlands (Ortner et al., 1999). Hrdlickas early 20th
century preferential bias for collecting pathological remains from
the surfaces of looted cemeteries quite likely skewed this gure upwards in the NMNH collection. In contrast, the very low
prevalence reported here is calculated from samples that were
generated mostly through attempts at regional representative
sampling strategies (and see below).
43
6. Conclusion
This study establishes the presence of scurvy in this region of the
South American Andes. However, scurvy appears as a rare disease
condition on the north coast of Peru. This work has underscored
careful description and differential diagnosis between multiple discrete sites in both the cranial and postcranial skeleton, the potential
co-morbidity between scurvy and rickets, and that ectocranial vascular impressions are consistent with scurvy. Also, it is argued that
identication of subadult hemarthoses deserves greater focus. The
future of research into the history, distribution, and signicance of
scurvy on the north coast of Peru is promising, as this disease represents an increasingly important component of paleopathological
reconstructions of Andean dietary adaptation, nutrition, and health.
Acknowledgements
Grants from the National Science Foundation (Grant BCS
1026169), the Wenner-Gren Foundation for Anthropological
Research (Grants 7302, 8009, 8132) and Utah Valley Universitys
College of Humanities and Social Sciences, The Center for Engaged
Learning, SCOP program, Presidential Scholar Award, Department
of Behavioral Science, and the International Center funded this
work from 2004 to 2012. I thank Peruvian project co-director
Rosabella Alvarez-Caldern (Harvard University) and all the contributors of the Lambayeque Valley Biohistory Project from Peru,
Japan, Canada, and the United States. Special thanks are owed
to Brian Birch, Steven Clark, Carlos Elera, Marco Fernndez, Juan
Carlos Wester, and David
Martnez, Raul Saavedra, Fausto Saldana,
Yells for their many contributions supporting this work. Scott
Applegate, Jenna Hurtubise, Marisa McKane, and Becky Ann Talpas worked out details of lesion patterning in the lab, while Judith
Arnett provided initial observations of lesions in CNS U4AE-2
during excavation. Figures 613 by Sam Scholes. I am grateful
to the editor, associate editor, Simon Mays, John Crandall, Clark
Larsen, Kate Teel, and the anonymous reviewers for their thoughtful
and constructive comments and corrections. Any remaining shortcomings are my own.
Most of all, I owe a debt of deepest gratitude to Don Ortner
for energizing my interest in scurvy (and for all the pathological
conditions of the human skeleton). This work is dedicated to his
memory.
Appendix A. Supplementary data
Supplementary data associated with this article can be found, in
the online version, at doi:10.1016/j.ijpp.2013.09.002.
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Brning, E., 1922 [1989]. Estudios Monogrphicas del Departmento de Lamabyeque.
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Chiclayo.
de la Ciencia, Cultura, y Atre Norteno,
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Donnan, C.B., 1989. En busca de Naylamp: Chotuna Chornancap y el valle de Lambayeque. In: Antonio de Lavalle, J. (Ed.), Lambayeque. Coleccion Arte y Tesoros
del Peru. Banco del Credito, Lima, pp. p.105p.136.
45
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Sixteenth-Century Peru. Stanford University Press, Stanford.
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Diagnosis of Bone and Joint Disorders. , 3rd ed. W.B. Saunders, Philadelphia, pp.
22472266.
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Rowe, J.H., 1948. The Kingdom of Chimor. Acta Am. 6, 2659.
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