In our study, we demonstrated that chronic inflammation was inversely related to the incidence of PCa. We concluded that inflammation of prostate puncture tissue may reduce the probability of malignant transformation of prostate gland epithelium. At present, inflammation was an important factor in the occurrence and development of many malignant tumors. Cervical cancer, HCC, esophageal cancer, and gastric cancer all have clear models about the relationship between inflammation and tumor progression. However, the specific relationship between inflammation and the occurrence and progression of PCa remains unclear. Gurel et al found that chronic inflammation was associated with a higher incidence of PCa , while large clinical trial data reported by Moreira et al presented that chronic inflammation was independently associated with low incidence risk of PCa . Besides, there were some researches showed that inflammation might not play a role in the incidence of PCa [12–14]. We had recognized that chronic inflammation in the prostate may cause proliferative inflammatory atrophy (PIA) and that PIA was associated with high-grade prostate intraepithelial neoplasia (HGPIN). Bills et al found that PIA enhanced the progression of PCa , while Brasil et al evaluated 100 radical prostatectomy specimens and found there was no significant association between PIA and PCa. Coussens et al proposed the close connection between chronic inflammation and gastric, liver, colon, and bladder cancer. For suppressing the inflammatory response, the risk of tumorigenesis could be further reduced. Deu to chronic inflammation was related to oxidative stress-mediated by the cyclooxygenase gene pathway, inhibiting this pathway may reduce the risk of cancers. Observational studies of PCa suggested that NSAID might play a protective factor in reducing the incidence of PCa. However, the protective effects of NSAIDs had been challenged and questioned in other studies, they had shown an increasing risk of PCa after taking NSAIDs [18, 19]. Therefore, our conclusion still needed to be further verified, and we should consider whether there was a difference in the impact of inflammation on prostate cells in different ranges of PSA levels.
There are several limitations to the present study. First, The number of subjects included in this study is small, and a large number of multicenter studies are still needed to confirm our conclusion. Also, we only found that inflammation may affect the incidence of PCa, but did not further consider whether the inflammation affected the occurrence of Gleason score. In addition, we only selected patients with patients with PSA 4-50ng/ml for study, and did not conduct stratified study on different PSA range.