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Volume 54, Issue 12, Pages 1128-1135 (December 2009)


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Histochemical localization of neutral proteases released during development of rat periradicular lesion

Masahito Tsuji, Masahiro YamasakiCorresponding Author Informationemail address, Kazuharu Amano, Hironori Matsui, Taisuke Morimoto, Hiroshi Nakamura

Accepted 15 October 2009.

Abstract 

Objective

The purpose of the present study was to examine the role of various neutral proteases released during the development of periradicular lesion.

Design

This lesion produced by pulpal exposure of mandibular first molar in rat. The histological and histometrical changes in periapical tissue examined. The presence of neutrophil elastase, cathepsin G, collagenase 2, gelatinase B, and secretory leukocyte protease inhibitor (SLPI) was immunohistochemically evaluated in the periapical tissue.

Results

After pulpal exposure, some inflammatory cells were present in the periapical tissue at 7 days, and periapical inflammation gradually increased. Alveolar bone resorption observed after 14 days and apical abscess found after 21 days. After 14 days, the area of periradicular lesion significantly increased compared from normal one (p<0.05). Neutrophil elastase, cathepsin G, collagenase 2, and gelatinase B were detected around the root apex at 14 days, then these proteases increased gradually and demonstrated in and around the abscess at 21 and 28 days. Morphologically, these protease-expressing cells are almost polymorphic and polynuclear shaped after 14 days. These cells significantly increased after 14 days compared from normal one (p<0.05). However, SLPI detected after 21 days around apical root. It significantly increased after 21 days (p<0.05).

Conclusions

These results suggested that neutrophil elastase, cathepsin G, collagenase 2, and gelatinase B induce the destruction of periapical tissue. We demonstrated that these neutral proteases released play an important role in development of periradicular lesion.

Department of Endodontics, Aichi-Gakuin University School of Dentistry, 2-11 Suemori-dori, Chikusa-ku, Nagoya 464-8651, Japan

Corresponding Author InformationCorresponding author. Tel.: +81 52 759 2148; fax: +81 52 754 2299.

PII: S0003-9969(09)00256-8

doi:10.1016/j.archoralbio.2009.10.003


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