Pulpasmärta och dentinsmärta kan orsaka patienten avsevärda besvär, och många faktorer påverkar utvecklingen av smärtan och hur länge den kvarstår. Diagnos och behandling är därför ofta ett problem för tandläkaren. Goda kunskaper om de underliggande strukturerna och smärtmekanismerna är en förutsättning för lyckad smärtbehandling.

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-fibermediated 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 diffcult 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 lling 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.