Calcific bursitis  may occur in isolation or in association with calcium hydroxyapatite deposits in a tendon/myotendinous junction (calcific tendinitis). In the latter scenario, which some might argue is always the scenario, the calcium hydroxyapatite crystals erode into an adjacent bursa. In the bursa, an intense inflammatory reaction is typically incited which may lead to liquefaction (into milk of calcium) of the calcific mass, as demonstrated in this case.

Uniquely however, in this case it is difficult to make a convincing argument for the rotator cuff damage that would be expected to be seen with previous calcific tendinitis. Given the odd pattern of presumable calcifications in the greater tuberosity (low on T1 & T2, however occult on the radiographs) this was likely the case, as the crystals can migrate into the humerus just as they can into the bursa.