PulpaDentinInterfaces

PulpaDentinInterfaces is a term used to describe the dynamic biophysical and cellular zone at the boundary between dental pulp and dentin. It comprises the dentin–pulp complex, including predentin, dentin with its tubules, the odontoblastic layer and their processes, dentinal fluid, and the surrounding pulp tissue and extracellular matrix. The interface coordinates nutrition, sensation, immune surveillance, and tissue remodeling in the dentin–pulp unit.

Anatomy and cellular organization: Odontoblasts line the pulp–dentin boundary and extend processes into dentinal tubules, secreting predentin that mineralizes into dentin. Dentinal tubules traverse intertubular dentin and contain fluid and odontoblastic processes. The dentin matrix carries growth factors such as TGF-β and BMPs trapped within mineral and released during demineralization. The pulp contains fibroblasts, mesenchymal stem cells, blood vessels, nerves, and resident immune cells.

Physiological roles: The interface provides nutritional support and waste exchange via dentinal fluid, contributes to sensory transduction through hydrodynamic stimulation of nerve fibers, and acts as a selective barrier controlling diffusion of fluids and molecules. It also serves as a reservoir of bioactive molecules that can modulate repair.

Repair and response to injury: In caries or insult, demineralization frees growth factors; odontoblasts may form reactionary dentin, while progenitor cells differentiate to form reparative dentin or tertiary dentin, helping seal the pulp.

Clinical relevance: Maintaining the health of the PulpaDentinInterfaces is a goal of conservative dentistry. Pulp exposure or extensive caries necessitates therapy; materials such as calcium hydroxide and mineral trioxide aggregate promote dentin bridge formation and bioactivity at the interface, and bonding systems aim to create durable adhesion to dentin while preserving pulpal vitality.

Aging and pathology: Dentin sclerosis and reduced tubule permeability alter the interface; inflammation can modify the cellular environment and dentin–pulp signaling, influencing healing potential.