PURPOSE: We provide an overview of some of the basic, clinical and epidemiological research that has been conducted to investigate the potential role of chronic inflammation in prostate carcinogenesis and to provide direction for future research on this hypothesis. MATERIALS AND METHODS: We reviewed the literature on this topic. RESULTS: Chronic inflammation has long been linked to cancers with an infectious etiology, such as stomach, liver and colon cancer, in patients with inflammatory bowel disease. Whether intraprostatic inflammation contributes to prostate carcinogenesis is unknown. Inflammation is frequently present in prostate biopsies, radical prostatectomy specimens and tissue resected for treatment of benign prostatic hyperplasia. Also, inflammatory infiltrates are often found in and around foci of atrophy that are characterized by an increased proliferative index. These foci, called proliferative inflammatory atrophy, may be precursors of early prostate cancer or may indicate an intraprostatic environment favorable to cancer development. Epidemiological studies have indirectly examined the role of chronic inflammation in prostate carcinogenesis through studies of pro-inflammatory and anti-inflammatory factors. When taken together studies of sexually transmitted infections, clinical prostatitis, and genetic and circulating markers of inflammation and response to infection hint at a link between chronic intraprostatic inflammation and prostate cancer. CONCLUSIONS: Additional well-designed basic, clinical and epidemiological studies are needed to resolve questions about the role of chronic inflammation in prostate carcinogenesis and to determine if intraprostatic inflammation is a rational target for chemoprevention.
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