DNA integrity and stability are essential to life. However, it has been estimated that an individual cell can suffer up to one million DNA changes per day. The relation between inflammation and DNA damage is well established. Activated neutrophils and macrophages produce a vast spectrum of endogenous reactive oxygen and nitrogen species (ROS and RNS, respectively) in a process termed respiratory burst. During chronic inflammation, the overwhelming persisting ROS production damages DNA. Apart from direct nucleotide lesions generated by inflammatory ROS, secondary mutagenic radicals (aldehydes, epoxides, lipid hydroperoxides) can also arise from ROS-mediated oxidation of other cellular macromolecules and can induce further DNA lesions. Besides DNA damage, pain is also triggered by inflammatory process. Investigating the interplay between inflammation, pain, and DNA damage/replicative stress is a challenge of this project. During CeTICS development, we consolidated models of inflammation and pain with which we are investigating causes and consequences of DNA damage. Also, we standardized different approaches to investigate DNA damage/replicative stress.