Apical periodontium response to enamel matrix derivative as an intracanal medication in rat immature teeth with pulp necrosis: radiographic and histologic findings.

INTRODUCTION: The aim of this study was to evaluate the enamel matrix derivative (EMD) biomaterial in nonvital immature teeth. METHODS: To arrest root development, pulpectomies were performed in the lower first molars of 36 4-week-old rats; the cavities were left exposed to the oral environment for 3 weeks. Then, chemical disinfection was performed, and triple antibiotic paste (TAP) or EMD was applied in the root canals. A control group did not receive any treatment. Radiographic and histological data were evaluated after 3 and 6 weeks. RESULTS: At 3 weeks, TAP promoted a milder inflammatory response and increased root lengths compared with the control group. At 6 weeks, root development and reduced periapical lesions could be observed in both test groups, mainly because of the deposition of a cementum-like tissue. EMD promoted narrower canals compared with TAP (P < .05). CONCLUSIONS: EMD deserves attention as a potential tool in the treatment of nonvital immature teeth. The ingrowth of cementum-like tissues into canal spaces favored dental wall thickness and may contribute to tooth resistance and support.

Sequential chemotactic and phagocytic activation of human polymorphonuclear neutrophils.

Human polymorphonuclear neutrophils (PMN) chemotax to a foreign entity. When the chemoattractants' origins are reached, specific receptors bind to the invader's surface, initiating phagocytosis, phagosome formation, and fusion with granule membranes, generating the bactericidal oxidative burst, and releasing lytic enzymes, specific peptides, and proteins. We explored the initial signaling involved in these functions by observing naïve, unprimed PMN in suspension using fluorescent indicators of cytoplasmic signals (Delta[Ca(2+)](i) and DeltapH(i)) and of bactericidal entities (oxidative species and elastase) exposed to N-formyl-methionyl-leucyl-phenylalanine (fMLP) and/or multivalent immune complexes (IC). fMLP and IC each initiate a rapid transient rise in [Ca(2+)](i), mostly from intracellular stores, simultaneously with a drop in pH(i); these are followed by a drop in [Ca(2+)](i) and a rise in pH(i), with the latter being due to a Na(+)/H(+) antiport. The impact of a second stimulation depends on the order in which stimuli are applied, on their dose, and on their nature. Provided that [Ca(2+)](i) is restored, 10(-7) M fMLP, previously shown to elicit maximal Delta[Ca(2+)](i) but no bactericidal functions, did not prevent the cells' responses with Delta[Ca(2+)](i) to a subsequent high dose of fMLP or IC; conversely, cells first exposed to 120 mug/ml IC, previously shown to elicit maximal Delta[Ca(2+)](i) and bactericidal functions, exhibited no subsequent Delta[Ca(2+)](i) or DeltapH(i) to either stimulus. While exposure to 10(-7) M fMLP, which saturates the PMN high-affinity receptor, did not elicit bactericidal release from these naïve unprimed PMN in suspension, 10(-5) M fMLP did, presumably via the low-affinity receptor, using a different Ca(2+) source.