A re-evaluation of localized hypoplasia of the primary canine as a marker of craniofacial osteopenia in European Upper Paleolithic infants.

Localized hypoplasia of the primary canine (LHPC) occurs in prehistoric and contemporary populations with prevalence varying from 0 to 89%. One of the highest prevalences ever reported is Upper Paleolithic infants from Europe where 70% are affected. In that LHPC is found in relatively high proportions of contemporary children with reported or suspected malnutrition, it is important to investigate the etiology of LHPC. Previous research indicates that LHPC occurs in two steps: craniofacial osteopenia results in temporary fenestration of the cortical bone overlying the primary canine crypt; secondly, minor physical trauma to the perioral region impacts on the unprotected forming tooth crown resulting in a small pit visible on the labial surface of the erupted tooth. Investigation of the prenatal diet of mothers whose children are shown later to have LHPC found mothers are significantly low in vitamin A. Hitherto an animal model for this problem has been lacking. Recently Newell and Skinner have recognized that LHPC occurs very commonly in orangutans. Recent study of infant jaws from Pongo pygmaeus (n=75) and Pan paniscus (n=39) shows all stages of fenestration and healing of the labial bone of the primary canine crypt. 85% of orangutan and 62% of bonobos show LHPC. Current research is directed at bioavailability of vitamin A to ape infants. LHPC is a marker of malnutrition; a common factor that could link orangutan and Upper Paleolithic mothers is low dietary fat intake. A minimal level of dietary fat is required for gut absorption of both vitamin A and carotenoids.