Hypoplastic pits on human deciduous canine teeth are attributed to nutritionally induced thinning of the crypt wall prior to eruption, exposing ameloblasts to unspecified physical trauma through the fenestration. Traditionally known as localized hypoplasia of the primary canine (LHPC), this little-understood condition is reported in fields ranging from public health to bioarchaeology. We propose the defect be termed a ‘crypt fenestration hypoplastic enamel defect’ (CFED) to reflect that an analogous lesion is created postnatally on maxillary molars of pigs. Pigs are accepted as a suitable proxy for many studies in human biology. We compare fenestration defects and CFEDs between 50 Sick Pen pigs, who died naturally, and 20 Controls. Observations were made of the presence, number and size of fenestrations in molar crypts. CFEDs were counted on erupted deciduous last molars and permanent first molars. Signs of being underweight and cranio-dental infection at death were recorded. Sick pen pigs show significantly more fenestrations at death and CFEDs acquired before death. These conditions co-occur with infection and poor growth. The deep fibers of temporalis muscle lie adjacent to the crypt wall of maxillary molars. We propose that contraction of this muscle during suckling and chewing creates large compressive forces against fenestrated bony surfaces sufficient to have physiological consequences for physically unprotected ameloblasts. While we conclude that a pig model is appropriate to study fenestration-induced enamel defects, this naturalistic experiment leaves unresolved whether osteopenia in pigs, and by extension in human infants, is due to disease and/or malnutrition.

ObjectivesTo examine the correspondence between histology of defective enamel and documented developmental stressors using a pig proxy; with the ultimate goal of differentiating, within enamel, stressor types including birth, weaning, surgery, and social disruption.Materials and methodsLower first molars were removed from five female and four male domestic pigs, thin‐sectioned and examined with phase‐contrast microscopy for daily and accentuated laminations. Known stressor events include birth; processing (nonanesthetized clipping of needle teeth, tail docking, and castration) within 5 days of birth; weaning in nursery; penned vaccination 2–4 days later; transfer to grower barn; additional vaccination. Timing of accentuated laminations was derived from counts of daily laminations from birth and between accentuated laminations; or, more commonly, from measurements between accentuated laminations divided by average daily lamination width.ResultsAcknowledging our small sample, we confirm daily periodicity of laminations in pig enamel. Lamination width varies among sexes (males wider), cusps, crown decile, and enamel depth (wider toward surface). Accentuated laminations occurred at reconstructed median ages of 3.7 days after birth (cf. up to 5 days for “processing”), 19.7 days (cf. 18–25 days for weaning), 4.5 days (cf. 2–4 days for vaccination) and ~39.5 days (cf. 63 days for transfer).DiscussionEncouragingly, the timing of known stressors (birth, surgical processing, weaning, and vaccination) can be determined with high precision, in good thin sections, from accentuated laminations in pig enamel. Timing of transfer was poorly estimated, likely reflecting lesser severity and the occurrence of undocumented stress events in the nursery.

Objectives: To compare relative response of enamel, dentin and bone to developmental stressors between attritional and catastrophic mortality assemblages of pigs.Materials and methods: Heads from 70 Sus scrofa of known sex, weight and age comprising an attritional sample of 50 sick pen (SP) pigs that died prematurely versus 20 control pigs slaughtered at 6 months (Catastrophic assemblage). Hard tissue changes (alveolar bone thinning), abnormal bone formation (Harris lines) and re-modeling (auditory bullae) were recorded. Areas and volumes of coronal enamel and dentin were recorded from microCT scans with Avizo 6.3 and Geomagic Wrap.