| dc.description.abstract | Atherosclerosis on head or neck artery is the primary cause of ischemic stroke which is the
leading cause of death at any age in Indonesia. In the last few years, chronic inflammatory due to
bacteria, such as pulpitis, has been known to play an important role in the onset of atheroschlerotic
pathogenesis. Pulpitis causes bacteremia which affects systemic inflammation. This condition may
lead to endothelial cells defunct, elevated oxidation, and lipid deposition which increases the risk of
aterosclerosis.
This research aimed to identify the formation of carotid atherosclerotic lesions in pulpitis rat
models.
Ten rat samples are divided into 2 groups: a control group (K) without treatment and a pulpitis
group (PU). The pulpitis group was established by inducing pulp perforation to the occlusal surface
of mandibular first molar teeth. The pulp cavity was then induced with 0.05 ml (0.5 McF) of
Streptococcus mutant, 3 times a week for 4 weeks. On the 29th day, rats were sacrified, their
carotid arteries were extracted and cross-sectionally cut. Histological preparations were performed
and colored by Picrosirius Red and Sudan IV. Histomorphometric analysis began with
morphological observation of carotid artery wall thickness, then statistically tested using
Independent T-test. Histomorphology analysis began with endhotelial disintegration, lipid deposition
and atheroma, then statistically tested using Mann-Whitney method.
The arterial walls of pulpitis group were significantly thicker 102,85 ± 3,37 µm than those of
control group (p<0.05). There is no significant difference in endothelial disintegration in each group.
The presence of lipid deposition and atheroma are seen at all samples in pulpitis group (100%).
Pulpitis increases the risk of carotid atherosclerosis | en_US |
