For bone marrow stromal cells (BMSC) to be useful in cartilage repair their propensity for hypertrophic differentiation must be overcome. A single day of TGF-β1 stimulation activates intrinsic signaling cascades in BMSCs which subsequently drives both chondrogenic and hypertrophic differentiation. TGF-β1 stimulation upregulatesSP7, a transcription factor known to contribute to hypertrophic differentiation, andSP7remains upregulated even if TGF-β1 is subsequently withdrawn from the chondrogenic induction medium. Herein, we stably transduced BMSCs to express an shRNA designed to silenceSP7, and assess the capacity ofSP7silencing to mitigate hypertrophy.SP7silencing dampened both hypertrophic and chondrogenic differentiation processes, resulting in diminished microtissue size, impaired glycosaminoglycan production and reduced chondrogenic and hypertrophic gene expression. Thus, while hypertrophic features were dampened bySP7silencing, chondrogenic differentation was also compromised. We further investigated the role ofSP7in monolayer osteogenic and adipogenic cultures, finding thatSP7silencing dampened characteristic mineralization and lipid vacuole formation, respectively. Overall,SP7silencing affects the trilineage differentiation of BMSCs, but is insufficient to decouple BMSC hypertrophy from chondrogenesis. These data highlight the challenge of promoting BMSC chondrogenesis whilst simultaneously reducing hypertrophy in cartilage tissue engineering strategies.