The kinetics and diffusion mechanism of surface-injected oxygen interstitials (O-i) in TiO2(1 1 0) were investigated using a microkinetics model in order to determine the effects of different conditions upon to the O-i reaction-diffusion network. Extended defects, whether incipient or pre-existing, may act as a source or sink for O-i. The present work uses a quantitative microkinetic model to describe this diffusion and reaction network based upon isotopic gas-solid exchange experiments. Pertinent outputs from the model determined that the activation barrier for surface injection of O-i is 2.4 eV, while dissolution of O-i from extended defect is 3.3 eV. The interstitial sequestration mechanism through extended defects leads to kinetic coupling effects that other sequestration mechanisms would not typically induce.