Sclerotinia sclerotiorum is a necrotrophic fungus causing devastating stem rot and associated yield losses of canola/rapeseed (Brassica napus) worldwide, including in Australia. Developing host resistance against Sclerotinia stem rot is critical if this disease in canola/rapeseed is to be successfully managed, as cultural or chemical control options provide only partial or sporadic control. Three B. napus breeding populations, C2, C5 and C6, including the parents, F1, F2, BC1P1 and BC2P2, were utilised in a field study with an objective of exploring the inheritance pattern of disease resistance (based on stem lesion length, SLL), the genetic relationships of disease with stem diameter (SD) or days to flowering (DTF), and to compare these new adult plant stem resistances against S. sclerotiorum with those of seedling (cotyledon and leaf) resistances in earlier studies. Heritability (broad-sense) of SLL, was 0.57 and 0.73 for populations C2 at 3 and 5 weeks post-inoculation, and was 0.21 for C5 at 5 weeks post-inoculation. Additive genetic variance was evident within all three populations for DTF but not for SD. Narrow sense heritability for DTF was 0.48 (C2), 0.42 (C5) and 0.32 (C6). SD, DTF and SLL were all inherited independently with no significant genetic covariance between traits in bivariate analysis. Genetic variance for SLL in populations C2 and C5 was entirely non-additive, and there was significant non-additive genetic covariance of SLL at 3 and 5 weeks post-inoculation. Generation means analysis in population C2 supported the conclusion that complex epistatic interactions controlled SLL. Several C2 and C5 progeny showed high adult plant stem resistance which may be critical in developing enhanced stem resistance in canola/rapeseed. While population C6 showed no genetic variation for SLL resistance in this study, it showed significant non-additive genetic variance at the cotyledon and leaf stages in earlier studies. We conclude that host resistance varies across different plant growth stages and breeding must be targeted for resistance at each growth stage. In populations C2, C5 and C6, resistance to S. sclerotiorum in stem, leaf and cotyledon is always controlled by non-additive effects such as complex epistasis or dominance. Overall, our findings in relation to the quantitative inheritance of Sclerotinia stem rot resistance, together with the new, high-level resistances identified, will enable breeders to select/develop genotypes with enhanced resistances to S. sclerotiorum.