Yes and no and maybe.
Yes because without any a priori information about the structure, you don’t know if there is a relationship between Tb.Th and Tb.Sp. You could have thin sparse struts or thick densely packed struts, or anything in between, or the opposite (thick/sparse or thin/dense). At this point you could make a fair assumption of independence between Tb.Th and Tb.Sp.
No because once you know something about your structure the assumption of independence is less strong. If for example you have a baseline measurement of Tb.Th and Tb.Sp and then you are measuring the anabolic effect of exercise or the catabolic effect of disuse, you can expect that trabecular thickening will be accompanied by a concomitant reduction in space between trabeculae (and vice versa).
Maybe because even in the case where you have a baseline structure, the way the bone actually responds, and the way the spheres are fitted and averaged, may be unintuitive, or challenge your conceptual model. For example perforated plates, with the dominant Tb.Sp component measuring the space between plates, may thicken by filling up the perforations first, or the parts of the rod-like trabeculae that thicken (giving Tb.Th) might not be the same parts that limit the spheres in the marrow space that give Tb.Sp.
So, you don’t really know until you measure and then check how related the variables are in your data with a statistical test of correlation.