Developing a pig model for crypt fenestration-induced localized hypoplastic enamel defects in humans.

Area of Science:

• Paleopathology
• Comparative Anatomy
• Developmental Biology

Background:

• Localized hypoplasia of the primary canine (LHPC) is a poorly understood dental defect.
• It is traditionally attributed to nutritional deficiencies causing enamel hypoplasia via crypt wall thinning and fenestration.
• A similar defect occurs in pigs, suggesting a potential animal model.

Purpose of the Study:

• To propose a new term, 'crypt fenestration hypoplastic enamel defect' (CFED), for this condition.
• To investigate the occurrence of fenestrations and CFEDs in pigs as a model for human deciduous canine hypoplasia.
• To explore the potential role of temporalis muscle contraction in causing these defects.

Main Methods:

• Comparison of fenestration defects and CFEDs in 50 'Sick Pen' pigs and 20 control pigs.
• Recording the presence, number, and size of fenestrations in molar crypts.
• Counting CFEDs on erupted deciduous and permanent molars, alongside recording signs of poor growth and infection.

Main Results:

• Sick pen pigs exhibited significantly more fenestrations and CFEDs compared to controls.
• These defects were found to co-occur with signs of infection and poor growth in pigs.
• The deep fibers of the temporalis muscle are anatomically positioned to exert forces on the maxillary molar crypt wall.

Conclusions:

• The pig serves as an appropriate model for studying fenestration-induced enamel defects.
• Temporalis muscle contraction during suckling and chewing is a proposed mechanism for generating compressive forces leading to CFEDs.
• The study highlights the need for further research into the role of osteopenia, disease, and malnutrition in these defects.