Rotator cuff tear oxidative stress induces tenocyte apoptosis causing further rotator cuff tendon degeneration. A neural theory also exists that suggests neural overstimulation leads to the recruitment of inflammatory cells and may also contribute to tendon degeneration. Tears of the rotator cuff tendon are described as partial or full thickness, and full thickness with complete detachment of the tendons from bone. Shoulder pain is variable and may not be proportional to the size of the tear. Neer promoted the concept of three stages of rotator cuff disease. Stage I, according to Neer, occurred in those younger than 25 years and involved edema and
Rotator cuff tear hemorrhage of the tendon and bursa. Stage II involved tendinitis and fibrosis of the rotator cuff in 25- to 40-year-olds. Stage III involved tearing of the rotator cuff (partial or full thickness) and occurred in those older than 40 years. For surgical purposes, tears are also described by location, size or area, and depth. Further subclasses include the acromiohumeral distance, acromial shape, fatty infiltration or degeneration of muscles, muscle atrophy, tendon retraction, vascular proliferation, chondroid metaplasia, and calcification. Again, in surgical planning, age-related degeneration of thinning and disorientation of the collagen fibers, myxoid degeneration, and hyaline degeneration are considered. However,