Biology Reference
In-Depth Information
Cranial and Orbital Roof Porosis and Differential Diagnosis
The reactive conditions of childhood that have become the mainstay of analytical paleo-
pathology are porotic hyperostosis and cribra orbitalia. These are descriptive labels and not
diagnoses. Some of the causes of porotic hyperostosis (vault) and cribra orbitalia (orbital
roof) are shared (
Walker et al., 2009; Oxenham and Cavill, 2010
). Which factor is the more
likely explanation for the porotic pitting seen in a skeletal sample depends on the origin
of the collection and the cultural and sociopolitical circumstance. For example, there is no
hereditary anemia in the Americas, but it should be considered when evaluating skeletal
samples where malaria is/was endemic (e.g., circum-Mediterranean or Southeast Asia)
(e.g.,
Borza, 1979; Hershkovitz et al., 1991; Sallares et al., 2004; Keenleyside and Panayotova,
2006
). However, the other causes should be carefully (and synergistically) assessed as
stresses such as folic acid deficiency during pregnancy, the ubiquity of common intestinal
worm infections (
Farid et al., 1969; Weiss and Goodnough, 2005
), and protein or calorie
malnutrition (Stuart-Macadam and Kent, 1992) can be differentially prevalent between
the sexes, between social classes, and between subsistence strategies (e.g.,
Vercellotti
et al., 2010
).
Vitamin C Deficiency and Scurvy
Parietal pitting and cribra orbitalia are part of a suite of cranial and postcranial reactive
changes that also occur in subadult scurvy (chronic vitamin C deficiency) and rickets (chronic
vitamin D deficiency). Therefore, the entire cranium as well as the postcranial skeleton
should be examined as these metabolic diseases can be differentially diagnosed. Vitamin C
(ascorbic acid), acquired solely from the diet (citrus fruits and cruciferous vegetables), is
an essential nutrient which, among other things, maintains cartilage and blood vessels,
acts as an antioxidant, fortifies the immune system, and facilitates iron absorption (
Stuart-
Macadam, 1989; Brickley and Ives, 2008
).
Chronic deficiency results in scurvy that in advanced clinical stages displays with subcu-
taneous hemorrhaging, open wounds, and loss of teeth, and, without metabolic intervention,
can result in death (
Brickley and Ives, 2008
). Scurvy has been differentially diagnosed in
several archaeological contexts (
Stuart-Macadam, 1989; Ortner and Erickson, 1997; Ortner
et al., 1999a, b, 2001; Brickley and Ives, 2006
). Features to look for to distinguish a case of
scurvy include cortex-penetrating pinpoint to penpoint sized pores (circa 0.5
e
1 mm) on
the greater wing of the sphenoid bone, the lateral zygomatic arches, alveolar area of the
maxilla, and/or the lambdoidal area of the occipital bone (
Ortner and Erickson, 1997; Ortner
et al., 1999a, b, 2001
) and scapulae (
Brickley and Ives, 2006
).
Vitamin D Deficiency and Rickets
In addition to parietal pitting and cribra orbitalia, rickets differentially displays with
abnormalities consistent with insufficient calcium that individually are nondiagnostic, but
collectively make a supportable case. The suite of characteristics consists of long bone shaft
deformities (bowing, flaring at the metaphyses), long bone growth plate deformities (rough-
ness, porosity, concavity or “cupping” of distal plates) and rib abnormalities (deformity,
porosity, and flaring at the costochondral joint) (
Ortner and Mays, 1998; Mays et al., 2006
).
Although rickets has been identified archaeologically (
Ortner et al., 2001
; Blondiaux et al.,
