Date of Completion

7-1-2016

Embargo Period

6-27-2017

Advisors

Dr. Chen, Dr. Kaufman, Dr. Safavi

Field of Study

Dental Science

Degree

Master of Dental Science

Open Access

Open Access

Abstract

Introduction: Apical periodontitis is characterized by inflammation and destruction of the periapical tissues that is primarily caused by polymicrobial infection of the pulp, which is dominated by Gram-negative species. Gram-negative bacteria have different virulence factors, e.g. cell wall endotoxin and serine lipids, which are toxic to the periapical tissues leading to activation of the host immune response and inflammatory reaction. Porphyromonas endodontalis (P.endodontalis), a Gram-negative bacterium, has been shown to populate necrotic root canal systems and may contribute to apical bone loss. Moreover, it is shown to synthesize novel serine dipeptide lipid classes (Lipid 654 and Lipid 430). Lipid 654 is significant increased in necrotic pulps whereas Lipid 430 remains at comparable levels between healthy and necrotic pulps of human teeth. This finding suggests that the Lipid 430 is likely not heavily involved in the inflammatory reaction of necrotic pulps. However, to date, the levels of lipid 654 and 430 in periapical tissues of teeth with apical periodontitis are still unknown. We hypothesize that the conversion of the lipids in the periapical tissue could be increased from that which is found in the necrotic tissue inside of the root canal space. We also evaluated the levels of prostaglandin E2 (PGE2) in these samples and the possible correlation with the levels of the serine dipeptide lipids.

Materials and methods: The lipid extracts from 12 extracted teeth (molars and incisors) with necrotic pulps with apical periodontitis were obtained from the necrotic apical pulpal tissues as well as from the periapical tissues of the same teeth. Third molars with vital pulps and intact premolars (n=12) were collected and processed as negative controls. PGE2, Lipid 654 and Lipid 430 were identified by liquid chromatography-multiple reaction monitoring mass spectrometry (LC-MRM MS).

Results: The Lipid 654 levels were significantly elevated in the teeth with pulpal necrosis versus healthy pulp contents, but no significant difference was seen in Lipid 654 levels between the canal and periapical samples for teeth with necrotic pulps. PGE2 levels detected in pulps and from periapical tissues of necrotic teeth with apical periodontitis increased significantly compared to the levels measured in the pulpal tissues from the same teeth. The ion abundances for Lipid 430 transitions were not detectable in most of the pulp and periapical samples.

Conclusions: Lipid 654 ions were elevated in teeth with necrotic pulps and apical periodontitis in the intracanal and periapical portions of the teeth, which supports its participation in the activation of the innate immune system. This elevation of Lipid 654 can also indirectly cause bone destruction associated with apical periodontitis. It is unclear at this time if the lipid species of Lipid 430 represent precursor or breakdown products (or both) for the constituent lipid species of Lipid 654. Elevated PGE2 levels in the apical samples of the teeth with apical periodontitis are in concordance with other studies showing the association of the PGE2 with bone destruction and inflammation.

Major Advisor

Dr. Frank Nichols

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