Colorectal cancer, one of the most prevalent malignancies globally with persistently high incidence and mortality rates, poses a significant threat to human health. However, its early detection rate remains relatively low, with many patients diagnosed at intermediate or advanced stages, resulting in suboptimal treatment outcomes and prognoses. Current research predominantly focuses on surgical interventions, while studies on cellular and molecular mechanisms remain limited. With the deepening research in tumor biology, the close relationship between inflammation and tumors has gradually been revealed. As a novel programmed cell death mechanism, cellular pyroptosis has attracted significant attention in tumor immunity and microenvironment regulation. This study systematically reviews the research progress on inflammatory carcinogenesis and cellular pyroptosis in colorectal cancer, analyzing their interaction mechanisms and the role of cellular pyroptosis in disease progression. The findings indicate that chronic inflammation regulates the transformation of undifferentiated cells into cancer stem cells through cytokines and growth factors, thereby constructing a procarcinogenic microenvironment. Cellular pyroptosis, triggered by inflammatory body activation and mediated by caspase family and gasdermin family proteins, exhibits dual effects: it promotes tumor cell death while influencing the tumor microenvironment through the release of cytokines such as IL-1β and IL-18. Targeting strategies for inflammatory carcinogenesis and cellular pyroptosis demonstrate therapeutic potential. This study provides theoretical foundations at the cellular and molecular levels to understand colorectal cancer pathogenesis, lays the groundwork for developing precision-targeted therapies, and facilitates the transition of colorectal cancer treatment from surgery-focused approaches to multi-mechanism combined interventions, ultimately improving patient prognosis.