Microbiologically induced calcite precipitation (MICP) is widely investigated for soil improvement, surface consolidation, and self-healing concrete, yet concrete crack sealing often fails not because calcium carbonate cannot form, but because precipitates are produced at poorly connected locations. In ureolytic systems, Sporosarcina pasteurii and related bacteria raise pH and carbonate alkalinity by hydrolyzing urea, while calcium supplies drive supersaturation. The extracellular polymeric substance (EPS) matrix around cells and biofilms is therefore not a passive coating; it can bind Ca2+, retain water and enzymes, shape diffusion gradients, and provide nucleation sites for calcite or metastable CaCO3. This mini review differs from broader MICP reviews by examining EPS control of mineral localization and bonding in concrete cracks. Representative studies report closure of 0.46-mm cracks after 100 d vs. 0.18 mm in controls and urea-hydrolysis constants of 0.09–0.91 d−1 between 10 °C and 20 °C. Evidence supports EPS effects on crystal morphology, distribution, and attachment, but causal proof within concrete cracks remains limited. We summarize how EPS chemistry and biofilm architecture affect local carbonate nucleation, how concrete crack conditions modify this process, and which measurements can separate EPS templating from bulk solution precipitation. We also compare ureolysis with other carbonate-forming pathways; adhesion, hydration, and cation binding may generalize, whereas kinetics and by-products are pathway-specific. The main implication is that MICP protocols should be evaluated by mineral localization and bonding quality, not only by total CaCO3 yield.