Authors: Seltzer S, Naidorf IJ.
Title: Flare-ups in endodontics: I. Etiological factors.
Journal: J Endod
Date: Nov 1985
Citation: 11(11):472-8
Category: Endodontic Emergencies
Evidence-based Ranking: 5
Purpose/Objectives: To discuss possible hypotheses of endodontic “flare-ups”

Discussion: 1.) Alteration of the local adaptation syndrome-the idea of an adapted area being exposed to a new irritant and resulting in a violent reaction leading to liquefaction necrosis 2.) Changes in periapical tissue pressure- the idea that either positive or negative pressure can lead to excess exudate and pressure on nerve endings or collection of factors periapically that will not drain respectively. 3.) Microbial factors-Gram – bacteria contain endotoxin which can activate Hageman factor which in turn leads to the production of bradykinin, a potent pain mediator. In addition endotoxin can activate the alternative pathway of the complement system; enhancing inflammation. Gram + bacteria contain teichioc acids are known to be potent immunogens, producing humoral antibodies. 4.) Effects of chemical mediators- such mediators include histamine, serotonin, prostaglandins, leukotrienes, and platelet activating factors. The effects are complex and usually intertwined. 5.) Changes in cyclic nucleotides- the role of cyclic AMP and GMP are usually opposite in regards to immune responses and neurotransmission, with c AMP down regulating these responses. 6.) Immunological phenomena- Both humoral immunity and cell mediated immunity play roles. IgG and IgE can result in an Arthus-type reaction and an immediate hypersensitive reaction respectively. 7.) Various psychological factors- these factors can influence the pain perception and reaction threshold.

Reviewer’s Comments: Classic in depth review of possible factors involved in flare-ups. Many of the categories overlap under immune/inflammatory responses; however the discussion is very detailed and descriptive