{'fraction_non_alphanumeric': 0.011347517730496455, 'fraction_numerical': 0.0, 'mean_word_length': 5.472477064220183, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The biology of rotator cuff tears

Purpose of review The aim of this review is to summarize recent developments in basic science that have improved our understanding of rotator cuff tears. Recent findings The concept of outlet impingement as the primary causative factor for rotator cuff tears has been challenged in recent years. Although impingement may play some part, the pathologic effects of overuse appear to be more significant in the development of rotator cuff tendinopathy. Overuse can cause an imbalance between tendon degeneration and repair resulting in overproduction of matrix metalloproteases, increased tenocyte apoptosis, and conversion of the tendon into a biomechanically inferior fibrocartilage. This can lead to attritional tears of the rotator cuff and mechanical failure. Aging appears to magnify the pathologic effects of overuse. Once the rotator cuff is torn, the musculotendinous unit undergoes further pathologic changes that may diminish the healing ability of rotator cuff repairs. These pathologic changes include decreased cellular activity within the tendon, chondroid metaplasia, and fatty atrophy of the muscle. Summary Rotator cuff disease involves a complex series of pathologic biochemical and biomechanical changes that appear to develop in response to overuse. Further study in the pathogenesis of rotator cuff disease may help guide treatment modalities in this area.