Abstract
This study further investigated the mechanisms underlying the rat model of tooth pulp inflammatory pain elicited by complete Freund’s adjuvant (CFA), in comparison to other pulpitis models. Pulps of the left maxillary first molars were accessed. In the CFA group, the pulps were exposed, and CFA application was followed by dental sealing. In the open group, the pulps were left exposed to the oral cavity. For the closed group, the pulps were exposed, and the teeth were immediately sealed. Naïve rats were used as negative controls. Several parameters were evaluated at 1, 2, 3 and 8 days. There was no statistical significant difference among the groups when body weight variation, food or water consumption were compared. Analysis of serum cytokines (IL-1β, TNF or IL-6) or differential blood cell counts did not reveal any evidence of systemic inflammation. The CFA group displayed a significant reduction in the locomotor activity (at 1 and 3 days), associated with an increased activation of satellite glial cells in the ipsilateral trigeminal ganglion (TG; for up to 8 days). Amygdala astrocyte activation was unaffected in any experimental groups. We provide novel evidence indicating that CFA-induced pulp inflammation impaired the locomotor activity, with persistent activation of ipsilateral TG satellite cells surrounding sensory neurons, without any evidence of systemic inflammation or amygdala astrogliosis.
Highlights
Dental pain associated with tooth pulp inflammation is very common
The body weight gain was slightly reduced in animals of open, closed and complete Freund’s adjuvant (CFA) groups from days 1 to 3 after pulp access (Fig 4A), the differences were not statistically significant when compared to the naïve controls (P > .05)
No significant difference was detected when comparing the food consumption/day/animal in any experimental time, an apparent reduction can be observed at day 1, in all the groups with tooth pulp access (P > .05; Fig 4C)
Summary
Dental pain associated with tooth pulp inflammation is very common. There were great advances concerning the identification of biomarkers associated with inflammatory pulp pain [1,2]. Classical rodent models of tooth pulp inflammation involve the pulp exposure, with or without the application of phlogistic agents such as formalin, mustard oil, capsaicin, or bacterial lipopolysaccharide (LPS). These models have been essential to elucidate diverse peripheral and central mechanisms underlying dental pain and trigeminal nociceptive transmission [3,4,5,6]. The knowledge regarding the different models of inflammatory dental pain is still incomplete and further experimental studies on this topic are required.
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