Evidence of Bone Remodeling in the Mandible of Domestic Pigs

Objective: The existence of secondary intracortical osteonal bone remodeling in the pig jaw has not been quantified using dynamic histomorphometry.

Method: Four female domestic American Yorkshire pigs (~two years old) received two pairs of calcein bone labels (12.5mg/kg) 7 days apart.  After sacrifice, bone sections were made through the dentate regions of the mandible and mid-femoral diaphyses.  A total of 16 sections (2 sections/bone site/animal) were quantified under epifluoresence using dynamic histomorphometric analyses for mineralizing surface/ bone surface (MS/BS, %), mineral apposition rate (MAR, µm/d), and bone formation rate (BFR, %/y). BFR is a product of MAR and MS/BS and is the main variable of interest as it represents remodeling. Remodeling was measured in the cortical regions and alveolar bone proper of the mandible and in the femur. The femur sections demonstrated large regional variations in remodeling with plexiform bone being nearly devoid of osteons. Thus the plexiform and remodeling regions in the femur were sampled separately and then averaged to determine the femoral BFR.  Data was sampled from the bone sections and analyzed statistically (ANOVA).      

Result: The mean (SD) of the BFR (%/yr) for the skeletal sites were as follows:  femur 54.0(±21.7); mandible 17.9(±5.0); mandibular alveolar bone proper 31.2(±7.7); mandibular cortical plates 22.4(±11.5).   The BFR in the femur was significantly (P<0.05) higher than in the mandible. There were no significant differences (p>0.05) in the BFR between the alveolar bone proper and cortical bone of the mandible. 

Conclusion: Intracortical osteonal bone remodeling exists in both the femur and in the mandible of the domestic pig model with levels comparable to the canine model. While each animal model poses benefits and challenges, understanding the fundamental differences in the dynamic histomorphometric bone turnover will advance our knowledge in choosing the most appropriate animal model for disease.