Photodynamic therapy (PDT) is used for cancer treatment based on the interaction of a photosensitizer (PS), light, and oxygen. The photodynamic interaction is termed type I and II depending on whether the cytotoxic oxygen species is through an electron transfer, producing oxygen superoxide and its secondary reactive oxygen species (ROS) or an energy transfer, producing singlet oxygen (1O2). Most photosensitizer exhibit both type I and II interactions. Explicit dosimetry of light fluence rate (ϕ), PS concentration ([PS]), and oxygen concentration ([3O2]) has been developed for clinic use, however, it is important to integrate these explicit quantities to a reacted ROS concentration, [ROS]rx. A mathematical model has been developed to incorporate the macroscopic kinetic equations for [ROS] generation, photosensitizers in ground and triplet states, 3O2, and tissue acceptors along with the Monte Carlo simulation for light transport in tissue. In this study, the ROSED model has been applied to type I (e.g., WST09) and several type II (e.g., HPPH, BPD, Photofrin) photosensitizers. Cure index was computed from the rate of tumor regrowth after treatment and was compared against three calculated dose metrics: total light fluence, PDT dose (product of light fluence and PS concentration), and measured and calculated reacted [ROS]rx. The tumor growth study demonstrates that [ROS]rx serves as a better dosimetric quantity for predicting treatment outcome, as a clinically relevant tumor growth endpoint. Values of threshold dose of [ROS]rx for type I and II interactions are discussed.