Porphyromonas gingivalis-induced alveolar bone loss is accelerated in the stroke-prone spontaneously hypertensive rat.

Abstract:

:Porphyromonas gingivalis (P. gingivalis) is one of the prominent periodontal pathogens and is the most important bacteria involved in the onset and exacerbation of periodontitis. P. gingivalis is an anaerobic, Gram-negative coccobacillus that plays a role in the progression of periodontal disease by promoting alveolar bone resorption. The aim of the present study was to examine P. gingivalis-induced osteoclastic bone resorption in the stroke-prone spontaneously hypertensive rat (SHRSP), in which oxidative stress induced by reactive oxygen species (ROS) is increased. In the present study, we used animals orally challenged with P. gingivalis as a chronic inflammation model. Horizontal bone loss around the maxillary molars was assessed morphometrically. Animals were divided into four groups: (1) P. gingivalis-non-infected Wister Kyoto Rat (WKY), (2) orally challenged with P. gingivalis WKY (WKY + Pg), (3) P. gingivalis-non-infected SHRSP, and (4) orally challenged with P. gingivalis SHRSP (SHRSP + Pg). Alveolar bone resorption was significantly increased in the orally challenged with P. gingivalis groups, and was accelerated in the SHRSP group. Histological analysis revealed that the infiltration of inflammatory cells was absent in all groups. However, the infiltration of osteoclasts was observed in the SHRSP + Pg and SHRSP groups. We examined P. gingivalis-induced alveolar bone loss in both the SHRSP and WKY. The results obtained demonstrated that P. gingivalis-induced alveolar bone loss would be involved in hypertension and stroke animal model, such as SHRSP and/or periodontal disease.

journal_name

Arch Oral Biol

journal_title

Archives of oral biology

authors

Tokutomi F,Wada-Takahashi S,Sugiyama S,Toyama T,Sato T,Hamada N,Tsukinoki K,Takahashi SS,Lee MC

doi

10.1016/j.archoralbio.2015.02.012

subject

Has Abstract

pub_date

2015-06-01 00:00:00

pages

911-8

issue

6

eissn

0003-9969

issn

1879-1506

pii

S0003-9969(15)00040-0

journal_volume

60

pub_type

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