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The pathogenesis of rotator cuff tears is multifactorial. Tendon abnormalities of the rotator cuff include alteration of collagen fiber structure, tenocytes, cellularity, and vascularity. Ruptured tendons show marked collagen degeneration and disordered arrangement of collagen fibers. Fibroblast population decreases as the size of the tear in the rotator cuff increases. The larger fibroblast population seen in the smaller tears is also actively proliferating and is part of an active reparative process. Inflammatory cell infiltrate correlates inversely to rotator cuff tear size in the torn supraspinatus tendon samples, with larger tears showing a marked reduction in all cell types. As tear size increase, there is also a progressive decrease in the number of blood vessels. Whether rotator cuff tear heals spontaneously is an important pathologic and clinical question. Histologic changes indicative of repair and inflammation lead to consider biological options in addition to biomechanical treatment of the rotator cuff tears.