The Upper Paleolithic Triple Burial of Dolnı Vestonice Pathology and Funerary Behavior
The Upper Paleolithic Triple Burial of Dolnı Vestonice Pathology and Funerary Behavior
The Upper Paleolithic Triple Burial of Dolnı Vestonice Pathology and Funerary Behavior
Department of Ethology, Ecology, and Evolution, University of Pisa, 56126 Pisa, Italy
Archaeological Institute, Czech Academy of Sciences, 66203 Brno, Czech Republic
KEY WORDS
ABSTRACT
This work focuses on paleopathological
analysis of one of the skeletons from the Gravettian triple
burial of Doln Vestonice (Moravia) and addresses issues
of Upper Paleolithic funerary behavior. The burial includes the well-preserved skeletons of three young individuals. The skeleton in the middle (DV 15) is pathological
and very problematic to sex; the other two (DV 13 and DV
14) are males and lie in an unusual position. The young
age, the possibility of a simultaneous interment, and the
position of the three specimens have given rise to speculations about the symbolic significance of this spectacular
and intriguing funerary pattern. The pathological condition of the skeleton in the middle further emphasizes its
peculiarity.
Main pathological changes of the DV 15 skeleton include:
asymmetric shortening of the right femur and of left forearm
bones, bowing of the right femur, right humerus, and left
radius, elongation of fibulae, dysplasias of the vertebral col-
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373
Epiphysial fusion and dental development indicate that these remains belong to a young adult
individual. In agreement with previous analyses (Vlcek, 1991, 1997; Jelnek, 1992), we suggest an age of
about 20 years. The same parameters yield a
slightly younger age (1719 years) for the other two
specimens, DV 14 being the youngest.
While based on morphology of well-preserved hip
bones a general agreement exists that DV 13 and 14
are males, the sex of DV 15 is problematic and
different determinations have been proposed by
Vlcek (1991), Jelnek (1992), and Novotny (1992). As
already pointed out by these authors, the main difficulty lies in an admixture of male and female characteristics exhibited by the pelvis, possibly linked to
the pathological state of the skeleton. Thus, a reliable sex diagnosis cannot be obtained on purely anatomical grounds.
The main pathological changes are mostly restricted to the postcranium and include:
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Fig. 2. Lower limb bones of DV 15: right (a) and left (b) femur in anterior view, right femur in lateral view (c), and right and left
fibulae and tibiae (d). Note shortening and bowing of right femur, varus deformation of its neck, and relative elongation of fibulae.
DIFFERENTIAL DIAGNOSIS
The early hypotheses
The skeleton of DV 15 has not yet been thoroughly
investigated from a paleopathological point of view.
However, two hypotheses have been proposed to explain the observed bone deformations:
1) hemiparalysis of the right side, possibly resulting
from encephalitis suffered in early life (Klma,
1987b); or
2) a rachitic condition (Jelnek, 1992).
Both diagnoses are unlikely. In particular, the
well-developed muscular insertions, the normal degree of lateralization, and the thickness of cortical
tissue argue against the first possibility, while the
absence of bowing of tibiae and fibulae, i.e., the
bones generally showing the most obvious manifestations of rickets, is inconsistent with the latter
diagnosis.
Another hypothesis has been suggested by Kuklk
(1992), who attributes the deformities of the right
femur to a congenital disease of poorly known etiology: proximal femoral focal deficiency (PFFD).
PFFD is a disease characterized by unilateral shortening of the femur due to failure of normal development of a portion of the proximal femur (Resnick,
1995a). Four classes of defects, based on femoral and
acetabular abnormalities, have been proposed (Aitken, 1969). In the milder forms (class A), the femur
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STONICE PATHOLOGY AND FUNERARY BEHAVIOR
Fig. 4.
molar.
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V. FORMICOLA ET AL.
Two patterns of malformations have been identified and referred to as caudal regression syndrome
(CRS) and femoral hypoplasia with unusual facies
syndrome (FH-UFS). Both result in postural deformities of the lower extremities, sometimes involving
asymmetric development of the femur (Johnson et
al., 1983; Guidera et al., 1991). However, the severity of femoral hypoplasia and its frequent association with radio-ulnar or radio-humeral synostosis
(Daentl et al., 1975) make a diagnosis of FH-UFS
very unlikely in DV 15. CRS is equally unlikely,
considering that this syndrome also involves sacral
agenesis of variable but generally severe intensity,
hip dislocations, and foot deformities (Resnick,
1995a).
The third syndrome, chondrodysplasia calcificans
punctata (CCP), is an inherited form of multiple
epiphysial dysplasia characterized by stippled calcifications in some areas of enchondral bone formation. Tubular bones, particularly the femur and humerus, and the vertebrae are among the most
frequently affected elements. The disease ranges
from a severe rhizomelic form resulting in stillbirth
or death within the first months of life to a milder
disorder, sometimes showing asymmetrical limb
shortening (Goldman, 1995). In cases of survival,
calcifications disappear by age 13 years (Hyndman
et al., 1976; Goldman, 1995), but there may be residual deformity. Correlation between severity of
stippling and residual deformity has been pointed
out (Comings et al., 1968; Spranger et al., 1971;
Silengo et al., 1980).
Different types of CCP have been recognized on
the basis of phenotype, mode of inheritance, and
gene defect localization (Goldman, 1995):
Rhizomelic, autosomal-recessive: lethal.
X-linked dominant (Conradi-Hunermann disease):
lethal for males, but associated with a good prognosis for females.
X-linked recessive (Curry type): normal survival.
X-linked recessive (Sheffield type): normal survival.
Tibia-metacarpal type: normal survival.
All the different types of CCP exhibit symmetric
shortening of the limbs, with the exception of the
X-linked dominant form, characterized by asymmetric involvement. Focal disruption of the growth
plate, varying from bone to bone, is the likely cause
of the asymmetrical nature of the changes (Rimoin
et al., 1976). The diagnosis is usually made during
the first year of life, based on the peculiar appearance of the newborn and radiographic examination.
However, despite the early disappearance of stippling, recognition of skeletal and soft-tissue anomalies allows diagnosis later in life (Comings et al.,
1968; Hyndman et al., 1976). The disease has a
highly variable clinical expression, as stressed by
many authors (Silengo et al., 1980; Manzke et al.,
1980; Mueller et al., 1985), who cite the existence
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