Cribra Orbitalia

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This refers to either active or healing lesions localized to orbital roof. These lesions tend to be in an active state of bony remodeling in children, whereas in affected adults these lesions have begun to heal over (Walker et al. 2009). In skeletal collections, the frequency of such lesions ranges from around 21% (Carlson et al. 1974) to 28% (Glen-Haduch et al. 1997, Wapler et al. 2004) in adults, and frequency across different age-groups ranges from 7.5 – 42% of individuals (Walker et al. 2009). While the condition has historically been identified in dry skulls, cribra orbitalia can also be identified in vivo with computed tomography (Exner et al. 2004).

The etiology of such cribra orbitalia is debated. There has been a tendency in the anthropological literature to view cribra orbitalia as an indicator of childhood nutritional stress. Specifically, many attribute such lesions to the expansion of the orbital marrow centers in response to iron deficiency (anemia), either dietary or hereditary (i.e. sickle cell or thalassemia). Recently, however, several lines of evidence suggest etiologies other than anemia for such orbital lesions. Glen-Haduch and colleagues (1997) found that skeletal individuals with and without orbital lesions did not differ in the levels of iron in their molars. This suggests that childhood anemia was not responsible for creating orbital lesions in this sample. In addition, Wapler and colleagues (2004) conducted histological study of the bony orbits of individuals exhibiting cribra orbitalia. Here, nearly half the lesions in the adult sample could be ascribed to anemia, while the rest were suggestive of either bony inflammation, pressure-induced bony atrophy, or hypervascularization. Finally, Walker and colleagues (2009) argued that cribra lesions reflect “subperiosteal hematomas” of the orbital roof in children. The authors state that scurvy (vitamin C deficiency) can weaken the connective tissue between the orbital bone and subperiosteum. Even minor trauma can cause separation of these two layers, which would cause subperiosteal bleeding and trigger bone deposition. Thus, the orbital lesions collectively termed ‘cribra orbitalia’ probably reflect multiple conditions and causes. Given the association with anemia as well as scurvy and rickets (iron, vitamin C and D, respectively), some sort of dietary deficiency probably plays some role in a majority of cribra orbitalia cases. Such dietary insufficiency could stem from restricted access to resources, or nutrient deficiency or malabsorption as would occur in the case of diarrheal disease (Walker et al. 2009).


Carlson DS, Armelagos GJ, Van Gerven DP. 1974. Factors influencing the etiology of cribra orbitalia in prehistoric Nubia. Journal of Human Evolution 3:405-10.

Exner S, Bogusch G, Sokiranski R. 2004. Cribra orbitalia visualized in computed tomography. Annals of Anatomy 186:169-72.

Gleń-Haduch E, Szostek K, Głab H. 1997. Cribra orbitalia and trace element content in human teeth from Neolithic and Early Bronze Age graves in southern Poland. American Journal of Physical Anthropology 103:201-7.

Walker PL, Bathurst RR, Richman R, Gjerdrum T, Andrushko VA. 2009. The causes of porotic hyperostosis and cribra orbitalia: a reappraisal of the iron-deficiency-anemia hypothesis. American Journal of Physical Anthropology 139:109-25.

Wapler U, Crubézy E, Schultz M. 2004. Is cribra orbitalia synonymous with anemia? Analysis and interpretation of cranial pathology in Sudan. American Journal of Physical Anthropology 123:333-9.

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