PMID- 23659424
OWN - NLM
STAT- MEDLINE
DCOM- 20141114
LR  - 20151119
IS  - 1943-3670 (Electronic)
IS  - 0022-3492 (Linking)
VI  - 85
IP  - 1
DP  - 2014 Jan
TI  - Toll-like receptor 4 expression in trigeminal neurons is increased during 
      ligature-induced periodontitis in rats.
PG  - 170-7
LID - 10.1902/jop.2013.130039 [doi]
AB  - BACKGROUND: Periodontitis, activated by oral bacteria and orchestrated by innate 
      immune response, is regulated by primary nociceptive neurons, which are generally 
      considered to have small- to medium-sized perikaryons. Bacterial byproducts 
      (e.g., lipopolysaccharides) activate primary nociceptive neurons directly through 
      Toll-like receptors (TLRs). Therefore, this study aims to morphometrically 
      characterize rat trigeminal neurons, which express TLR4, and to investigate the 
      changes in the TLR4 expression in neurons during periodontal inflammation. 
      METHODS: Trigeminal neurons innervating gingivomucosa were identified by 
      application of the retrograde tracer hydroxystilbamidine into the gingival sulcus 
      of the maxillary molar in 14 rats. Periodontitis was induced by ligature around 
      the same molar in seven rats. TLR4 expression was investigated by 
      immunohistochemistry on paraffin sections of the trigeminal ganglia (TG). 
      Semiquantitative method was used to identify the intensity of TLR4 expression. 
      RESULTS: In the control group without the ligatures, TLR4 was detected in 19% of 
      the neurons in the maxillary region of TG and in 29% of neurons innervating 
      gingivomucosa. Expression of TLR4 was more frequent and intensive in small- to 
      medium-sized neurons than in large-sized neurons. One week after ligature-induced 
      periodontitis, the percentage of TLR4-positive neurons in the maxillary region 
      and among the neurons innervating inflamed gingivomucosa significantly increased 
      statistically to 32% and 41%, respectively. CONCLUSIONS: TLR4 is predominantly, 
      but not exclusively, expressed in smaller trigeminal nociceptive neurons in the 
      rat. Experimental periodontitis upregulates TLR4 expression in the trigeminal 
      neurons. The hypothesis that bacterial byproducts regulate the pathogenesis of 
      periodontitis by activation of trigeminal nociceptors through TLR4 should be 
      explored.
FAU - Vindis, Bojan
AU  - Vindis B
AD  - Institute of Pathophysiology, Faculty of Medicine, University of Ljubljana, 
      Ljubljana, Slovenia.
FAU - Gaspersic, Rok
AU  - Gaspersic R
FAU - Skaleric, Uros
AU  - Skaleric U
FAU - Kovacic, Uros
AU  - Kovacic U
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130509
PL  - United States
TA  - J Periodontol
JT  - Journal of periodontology
JID - 8000345
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Stilbamidines)
RN  - 0 (Tlr4 protein, rat)
RN  - 0 (Toll-Like Receptor 4)
RN  - 39J262E49W (hydroxystilbamidine)
SB  - IM
MH  - Animals
MH  - Female
MH  - Fluorescent Dyes
MH  - Gingiva/innervation
MH  - Gingivitis/metabolism/pathology
MH  - Mouth Mucosa/innervation
MH  - Nociceptors/metabolism
MH  - Periodontitis/*metabolism/pathology
MH  - Rats
MH  - Rats, Wistar
MH  - Stilbamidines
MH  - Toll-Like Receptor 4/*analysis
MH  - Trigeminal Ganglion/*metabolism
EDAT- 2013/05/11 06:00
MHDA- 2014/11/15 06:00
CRDT- 2013/05/11 06:00
PHST- 2013/05/11 06:00 [entrez]
PHST- 2013/05/11 06:00 [pubmed]
PHST- 2014/11/15 06:00 [medline]
AID - 10.1902/jop.2013.130039 [doi]
PST - ppublish
SO  - J Periodontol. 2014 Jan;85(1):170-7. doi: 10.1902/jop.2013.130039. Epub 2013 May 
      9.