Abstract
Vascular endothelial growth factor (VEGF)-induced angiogenesis contributes to inflammatory bone resorption in humans. Widely documented antagonists to resorption include antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs). The purpose of this study was to investigate the effect of these drugs on proangiogenic VEGF levels in periradicular lesions. Periapical tissue biopsies were obtained from 42 patients with chronic periapical periodontitis. VEGF levels were measured using a commercial ELISA kit in patients divided into groups according to treatment: no drugs (control group, n = 25), NSAIDs (n = 7), antibiotics (n = 5), and NSAIDs and antibiotics (n = 5). Reverse transcriptase (RT) reaction was performed in all the samples under analysis. Presence of VEGFA and VEGFB gene expression was assessed using reverse-transcription-polymerase chain reaction (RT-PCR). ELISA analysis indicated that average VEGF levels in tissue samples of patients treated with NSAIDs (6.097 ± 1.930 ng/mL), antibiotics (5.661 ± 2.395 ng/mL), and NSAIDs and antibiotics (7.142 ± 2.601 ng/mL) were significantly lower than in samples of control patients (10.432 ± 4.257 ng/mL, ANOVA p = 0.008). The RT-PCR did not reveal VEGFA gene expression in any of the 42 samples. VEGFB gene expression was found in 26 of 42 samples (69.1%). The use of NSAIDs or antibiotics in patients with exacerbated chronic periodontitis decreases VEGF levels in periapical tissues. Pharmacotherapy may minimize the effects of VEGF on apical periodontitis progression in that way.
Highlights
In chronic periapical periodontitis, there is a dynamic balance between the bacteria in the canal system and the host response in surrounding tissues
ELISA analysis revealed that mean vascular endothelial growth factor (VEGF) levels in inflamed periapical tissue of patients in the three treatment groups were significantly lower than those of control patients, who did not take any drugs (10.4324 ng/mL, ANOVA p = 0.008)
Post-hoc analysis revealed that only the VEGF level in group III (NSAIDs and antibiotics) was not significantly different from the mean VEGF level in the control group (p = 0.07)
Summary
There is a dynamic balance between the bacteria in the canal system and the host response in surrounding tissues When this balance is disturbed, exacerbation occurs spontaneously with severe symptoms due to the local production of pro-inflammatory and immune factors. Histological and immuno-histochemical analyses confirmed that the application of topical ozone gas increases VEGF expression and, may be effective in the early stages of wound healing [6]. These findings suggest that VEGF is a significant signaling molecule in the communication between endothelial cells and osteoblasts [7]. Data about its role in periodontal lesions are still limited
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