Composition

Dentin has an average of 45,000-90,000 tubules/mm2 near the pulp, 30,000-35,000 in the middle and 10,000-25,000 at the periphery. At the pulp surface, the diameter of the tubules ranges from 2.5-3.0 μm and at the periphery to less than 1.0 μm. Each tubule is about 1 μm in diameter and 2.0-3.0 mm in length. The occluded dentinal tubules referred to as dentin sclerosis, react differently to acid etching. The etching time here is to be modified to provide an adequate hybrid layer of collagen and resin.

The interface dentin with irregular often atubular dentin forms a barrier between the physiologic secondary and tertiary dentin. This barrier reduces the permeability of the affected dentin and may make it impermeable because the tubules from primary dentin do not cross the interface dentin. This phenomenon protects the pulp.

Generally, dentin directly under the dentino-enamel junction is only 1.0% permeable, but permeability increases to 7.6% halfway to the pulp and up to 22.0% at the pulp surface. The pulpal circulation maintains an intercellular hydraulic pressure of about 24 mm of Hg, which causes the fluid flow in the tubules to be directed outwards from the pulp to the dentino-enamel junction.

Chemical and bacterial products when introduced into unprotected dentinal tubules diffuse against the pressure gradient towards the pulp. During cavity preparation by the operator, a layer is formed by the action of the cutting instrument on the calcified dentinal matrix called the ‘smear layer’. This mat of organic and inorganic particles obliterates the tubules to some extent but can be removed by acid etching and other means.

It is richly supplied by thin walled but wide capillaries. Bundles of myelinated nerve fibers accompany the blood vessels. Fibers predominantly present are collagenous and reticular fibers which lie in close proximity to the blood vessels along with many undifferentiated mesenchymal cells and histiocytes. These are believed to transform into secondary odontoblasts that form reparative dentin following the death of primary odontoblasts. When confronted with toxic bacterial or chemical products by way of dentinal tubules, the pulp usually responds initially by acute pulpitis. The response resolves naturally if the injurious agent is removed or its concentration lowered. If pulpitis does not resolve, it may spread to involve the pulp in liquefaction necrosis or chronic inflammation. Differentiation of secondary odontoblasts may eventually lead to formation of reparative dentin.