The character of parietal and orbital alterations in the superfamily Hominoidea (families Hominidae [exclusive of Homo] and Hylobotidae).

Abstract

Parietal external surface disruption routinely referred to as porotic hyperostosis, and orbital alterations (cribra orbitalia), have been attributed to anemia-related bone marrow hyperplasia in humans. A recent study in humans identified that they were actually vascular in nature. Skeletons were examined and epi-illumination surface microscopy was performed on the parietal region and orbit of 156 Hominidae and 123 Hylobotidae to assess if these phenomena were trans-phylogenetic. Trans-cortical channels were recognized on the basis of visualized ectocranial surface defects penetrating the parietal; cribra orbitalia, by alteration of the normally smooth orbital roof appearance. Trans-cortical parietal channels, ranging in size from 20 to 100 µm, are rare in Gorilla and Pan troglodytes and absent in Pan paniscus. They are universally present in adult Pongo abeli and in Hylobatidae, independent of species. Cribra orbitalia was common in Hylobotidae, Pongo pygmaeus and P. abelii, less prevalent in adult P. troglodytes, and not recognized in any Gorilla gorilla or P. paniscus examined. The proliferative form predominated, with the exception of Hylobates concolor and muelleri, in which uncalcified vascular grooves predominated. No correlation was observed between the presence of either trans-cortical channels or cribra orbitalia and fractures, osteoarthritis, or inflammatory arthritis. Parietal alterations observed in apes are trans-cortical channels, analogous to those observed in humans, and do not represent porosity. Similarly, cribra orbitalia in apes is confirmed as vascular in nature. The proliferative form apparently represents calcification of blood vessel walls, indistinguishable from observations in humans. Predominant presence in adults rather than in juveniles suggests that both forms are acquired rather than developmental in derivation. Sex and bone alteration/disease-independence suggests that mechanical, endocrine, and inflammatory phenomena do not contribute to the development of either. Further, independent occurrence of trans-cortical channels and cribra orbitalia suggests that they do not have a shared etiology.