What causes inflammation to be characteristically painful?

Inflammation is characteristically painful primarily due to the release of inflammatory mediators. When tissue is injured or infected, various cells, such as mast cells and macrophages, release substances like prostaglandins, bradykinin, and histamines. These mediators enhance the sensitivity of nerve endings in the affected area, leading to the sensation of pain.

Prostaglandins, for example, sensitize sensory neurons to other stimuli, which means that normally non-painful stimuli can cause pain when inflammation is present. This heightened sensitivity is especially important because it serves a protective function, alerting the body to the injury or infection and prompting behaviors that help to minimize further damage.

While fluid accumulation, tissue necrosis, and vascular engorgement can contribute to the overall inflammatory process and may lead to discomfort, it is the biochemical changes mediated by those inflammatory mediators that directly induce pain. This intricate interplay of cellular responses emphasizes the complexity of the inflammatory process and its role in alerting the body to potential threats.