Dental and Oral Biology

This is the most common reason. As a result of intrusion, pressure is there on the underlying tissues. Thus, chances of disruption of circulation are more.

In a study by Trevino et al, it was found that EDTA had 89% cell survival. It also had beneficial effects on pulp cells, when used as dentin conditioner.

Dendritic cells are the master regulators of immune system in pulp. When pulp is irritated, odontoblastic processes sense invasion and elicit requirement of dendritic cells which phagocytose invaders and present antigens to stimulate T-lymphocytes.

Phagocytes are released only when caries and pulp come in direct contact.

In pulpal diseases, the signs and symptoms of conditions make the basis for classification.

The response of normal uninflamed pulp is delayed when heat test is done.

Recent research has shown that sensory neuropeptide CGRP is responsible for an increase in blood flow during pulpal inflammation.

This is the most probable reason as with the application of heat, gases expand and cause pain.

Mast cells are cells of connective tissue. They release histamine in time of inflammation. But in normal pulp, unlike other connective tissues, mast cells are not there and appear only during inflammation.

If the temperature is maintained, response to cold decreases.

This is a radiopaque condition resulting in bone deposition and is considered as differential diagnosis of condensing osteitis.

All of the above are parts of pulpal classification.

Dentin is the protective casing of the pulp. Dentin removal will cause damage to the pulp.

Increased tissue pressure, inability of pulp to expand, lack of collateral circulation and low compliance system are the factors leading to pulp necrosis and periapical pathosis.

In acute apical abscess, the communication is not yet established with apical foramen and thus, drainage is usually not through the accessed tooth. Hence, both the statements are correct.