will respond to sensitiviity tests as a healthy pulp would. treatments include root canal or tooth extraction. in endodontic therapy, removal of the inflamed pulp relieves the pain. the empty root canal system is then obturated with gutta-percha (rubber material that acts as a pressure/pain reliever). pulp necrosis pulp necrosis is when the pulp has died/dying. causes include untreated caries, trauma or bacterial infection. it is often subsequent to chronic pulpitis. teeth with pulp necrosis undergo a root canal or extraction to prevent further spread of the infection, which may lead to an abscess. symptoms necrosis may be symptomatic or asymptomatic. symptomatic necrosis involves lingering pain response to hot and cold stimuli, spontaneous pain that may cause a patient to awaken during sleep, difficulty eating and senstivity to percussion. asymptomatic necrosis is non-responsive to thermal stimuli or electric pulp tests, leaving the patient unaware of the pathology. diagnosis asymptomatic necrosis is may go unnoticed by the patient and so a diagnosis may not be attempted. diagnosis may involve x-rays and sensitivity testing with. hot or cold stimuli (using warm gutta-percha or ethyl chloride), or an electric pulp tester. tooth vitality (blood supply) may be assessed using doppler flowmetry. sequelae of a necrotic pulp include acute apical periodontitis, dental abscess, or radicular cyst and tooth discolouration. prognosis and treatment untreated necrotic pulp may result in further complications, such as infection, fever, swelling, abscesses and bone loss. two treatment options are available for pulpal necrosis. pulp response to caries pulpal response to caries can be divided into two stages – pre- and post-infection. in caries-affected human teeth, odontoblast-like cells appear at the dentine-pulp interface along with specialized pulp immune cells to combat caries. once they identify specific bacterial components, these cells activate innate and adaptive immunity. in uninfected pulp, leukocytes can sample and respond to the environment, involving macrophages, dendritic cells (dcs), t cells and b cells. this sampling process is part of the normal immune response, as it triggers leukocytes from the circulatory system to adhere to endothelial cells lining blood vessels and then migrates to the site of infection for defence. macrophages can phagocytose bacteria and activate t cells, triggering the adaptive immune response that occurs in association with dcs. in the pulp, dcs secrete a range of cytokines that influence immune responses, and are key regulators of the infection defence. a comparatively small number of b cells are present in healthy pulp tissue, and pulpitis and caries progression increase their numbers. when bacteria get closer to the pulp but are still confined to primary or secondary dentine, acid demineralization of dentine occurs, producing tertiary dentine to help protect the pulp from further injury. after a pulp exposure, pulp cells are recruited and differentiate into odontoblast-like cells, contributing to the formation of a dentine bridge, increasing dentin thickness. the odontoblast-like cell is a mineralized structure formed by a new population of pulp-derived cells that can be expressed as toll-like receptors. they are responsible for the upregulation of innate immunity effectors, including antimicrobial agents and chemokines. one important antimicrobial agent produced by odontoblasts is beta-defensins (bds). bds kill microorganisms by forming micropores that destroy membrane integrity and cause leakage of the cell content. another is nitric oxide (no), a highly diffusible free radical that stimulates chemokine production to attract immune cells to the affected areas and neutralize bacterial by-products in pulp cells in vitro. pulp stones pulp stones are calcified masses that occur in the pulp, either in the apical or coronal portions. they are classified according to their structure or location. according to their location, pulp stones can be classed either as free (completely surrounded by pulp), embedded (surrounded by dentine tissue) or adherent (attached to pulp wall continuous with dentine, but not fully enclosed). depending on the structure, they are either true (dentine lined by odontoblasts), false (formed from degenerating cells that mineralise) or diffuse (more irregular in shape to false stones). the aetiology of pulp stones is little understood. it has been recorded that pulpal calcifications can occur due to: pulp degeneration increasing age orthodontic treatment traumatic occlusion dental caries pulp stones usually consist of circular layers of mineralised tissues. these layers are made up of blood clots, dead cells and collagen fibres. occasionally, pulp stones appear surrounded by odontoblast-like cells that contain tubules. pulp stones can reach as high as 50% in surveyed samples. pulp stones are estimated to typically range from 8–9%. pulpal calcifications are more common in females and more frequent in maxillary teeth compared to mandibular teeth. the reason is uncertain. they are more common in molar teeth, especially first molars compared to second molars and premolars. a review suggested this was because the first molars are the first teeth to be located in the mandible (lower jaw) and have longer exposure to degenerative changes. they also have a larger blood supply. in general, pulp stones do not require treatment. depending on the stones' size and location, they may interfere with endodontic treatment and should be removed. complications pulp acts as a security and alarm system. slight decay in tooth structure not extending to the dentin may not alarm the pulp, but as the dentin gets exposed, due either to dental caries or trauma, sensitivity starts. the dentinal tubules pass the stimulus to the pulp's odontoblastic layer, triggering the response. this mainly responds to cold. at this stage, simple restoration can be performed. as the decay progresses near the pulp, the response magnifies. sensation to heat and cold increases. at this stage, indirect pulp capping may be adviseable. at this stage it may be impossible to clinically diagnose the extent of decay. carious dentin by dental decay progressing to the pulp may get fractured during mastication, traumatizing the pulp, resulting in pulpitis. pulpitis can be painful and may call for root canal therapy or endodontic therapy. traumatized pulp starts an inflammatory response. the hard and closed surroundings builds pressure inside the pulp chamber, compressing the nerve fibres and eliciting pain. at this stage, the pulp starts to die, progressing to periapical abscess formation (chronic pulpitis). pulp horns recede with age. the pulp undergoes a decrease in intercellular substance, water, and cells as it fills with collagen fibers. this decrease in cells is evident in the reduced number of undifferentiated mesenchymal cells. the pulp becomes more fibrotic, reducing the regenerative capacity of the pulp due to the loss of these cells. the overall pulp cavity may become smaller by the addition of secondary or tertiary dentin and cause pulp recession. the lack of sensitivity associated with older teeth is due to receded pulp horns, pulp fibrosis, the addition of dentin, or all these changes. restorative treatment can be performed without local anaesthesia on older dentitions.