Sammanfattning
The specialized anatomy of the pulp-dentin complex
and the dense, predominantly nociceptive pulpal
innervation from the trigeminal nerve, explains
the variety of pain sensations from this organ.
Brief, sharp pain is typical of A-fiber-mediated
pain, whilst long-lasting, dull/aching pain indicates
C-fiber involvement. A-fibers react to cold or mechanical
stimuli, such as cold drinks or toothbrushing,
whereas C-fibers are mainly activated by inflammatory
mediators. Thus, lingering pain suggests
the presence of irreversible pulpal inflammation.
During pulpitis, structural changes of the pulpal
nerves (sprouting) occur and neuropeptide release
triggers an immune response; neurogenic inflammation.
Pain sensations during pulpitis can range
from hypersensitivity to thermal stimuli to severe
throbbing, or aching pains that can be referred and
often difficult to localize making diagnosis a challenging
situation for the clinician.
The surface biofilm amplifies hypersensitivity
of exposed dentin surfaces because irritants reach
the pulp through open dentin tubules, producing
inflammation. Removing the biofilm reduces dentin
hypersensitivity but supplemental treatment
aimed at reducing dentin permeability, is often
necessary. Caries removal and filling therapy is
adequate during reversible pulpitis if the pulp has
maintained its ability to distance itself from the
bacterial assault by producing reparative dentin.
However, endodontic therapy is necessary when
pulpitis has reached an irreversible stage.