It is also unlikely that this procedure would provide any more information than thermal and electric pulp sensibility tests. Therefore, test cavities are not generally used in practice as a means of testing pulp sensibility. Treatment
Once the pulp has become inflamed, the tooth can be diagnostically divided into two categories: reversible pulpitis and irreversible pulpitis

Reversible
This is the condition where the pulp is inflamed and is actively responding to an irritant. This may include a carious lesion that has not reached the pulp. Symptoms include transient pain or sensitivity resulting from many stimuli, notably hot, cold, sweet, water and touch. The pulp is still considered to be vital. This means that once the irritant is eliminated, usually by removal of decay and the placement of a restoration, that the pulp will return to its normal, healthy state. When it becomes painful and decayed the tooth may become known as a "hot tooth" and local anesthetic may not work as well. Irreversible
This is the condition where the pulp is irreversibly damaged. The pulp cannot recover from the insult and damage. For example, decay that has reached the pulp of the tooth introduces bacteria into the pulp.
Activated macrophages are effective killers that eliminate pathogens in both innate and adaptive immune responses, and are also important in tissue homeostasis, through the clearance of senescent cells, and in remodeling and repair of tissue after inflammation. The number of macrophages increases with the progression of caries and is always higher than that of DCs at all stages of the caries invasion. Neurological responses
According to the Brännströms hydrodynamic theory, activated nociceptors from fluid movement and other irritants through the patent dentine tubules result in pulp pain. Unmyelinated, slow conducting C-fibers aid in feeling a slowset, burning pain. According to neuronal studies, 70-80% of pulpal axons are unmyelinated. Highly myelinated Aδ-fibers, which allow for fast conduction, are responsible for the sharp, shooting pain.Thus, the stimulus intensities are based on various fibers. Fast-conducting Aβ and Aδ-fibers provide the lowest stimulus intensities (typically referred to as prepain sensations), and those sensations eventually receive higher stimulation levels. The dull aches are associated with C-fibers and slow Aδ-fibers. As inflammation intensifies, the A-fibers are increasingly activated. C-fiber innervation and Aδ-fibers are polymodal receptors that are sensitive to capsaicin and inflammatory mediators.The pain mechanisms associated with pulpitis are similar to those of the rest of the body (i.e. receptors, intracellular signaling, transmitters, etc.). The inflammatory mediators act on specific receptors relating to nociceptive neurons, leading to the production of second messengers and activation of phospholipases and protein kinases. The second messengers regulate receptors ion channels that deal with sensitization.