Objectives:
Dentin, deposited by odontoblasts, comprises the main portion of the tooth. Following the formation of primary dentin with tooth eruption, secondary dentin forms and continues to grow throughout life, resulting in narrowing the pulp canal. Tertiary dentin, on the other hand, forms in response to irritation or injury. We hypothesized that injury-induced tertiary dentin formation will be reduced/inhibited in the aged tooth due to reduced pulp stem cells.
Methods:
To test our hypothesis we employed young (2 months old) and aged (2 years old) male mice. Tooth injury was induced in the right mandibular first molar. Following anesthesia, the occlusal surfaces of the right mandibular first molars were injured halfway into the dentin layer using a No. 2 round bur drill, air-dried, and sealed with Cavit (Premier). Tertiary dentin was analyzed 4 weeks following injury using micro computed tomography (μCT) at 7.5 micron resolution. In each group we analyzed intact and injured molars from the same mouse.
Results:
As expected, dentin volume in the intact molars increased with age from 86.96±0.94% in young mice to 94.08±1.16% in aged mice. Similarly, dentin density increased from 1.24±0.02mg/cc in young mice to 1.35±0.02mg/cc in aged mice. In contrast, pulp volume decreased with age from 2.59±0.28% in young mice to 1.64±0.33% in aged mice. Enamel volume decreased by approximately 50% with age from 10.44±0.73% in young mice to 4.26±0.94% in aged mice, likely due to life long irritation (wear and tear). However, enamel density did not change with age. Surprisingly, preliminary data from the injured molars of the same mice revealed blunted tertiary dentin formation in aged mice, while injured molars in young mice showed variable volumes of tertiary dentin.
Conclusions:
These preliminary studies suggest complete depletion of stem cells in the aged pulp.