Fig. 1
The figure shows the hematoxylin and eosin staining of the rotator cuff tear (Å~5). Chronic inflammatory infiltrate, fibroblasts proliferation, and sclerosis, that are related to neoangiogenesis, are observable
Fig. 2
The figure shows a characteristic neoangiogenesis and fibroblast proliferation with collagen fibers displayed in random arrangement (E/E 20×)
Fig. 3
(a) Tendon: capillary proliferation and increased cellularity (H/E 109). (b) Tendon: chondral metaplasia: chondrocytes-like cells were either clustered in groups or randomly dispersed in the matrix (H/E 40×). (c) Tendon: collagen fibers appear discontinuous and disorganized (Masson’s trichrome 209). (d) Tendon: chondral metaplasia: alcian blue staining provides the histochemical demonstration of the presence of sulfated glucosaminoglycans (40×). (e) Bursa: bursal samples showed edema, capillary proliferation, and hypertrophy/hyperplasia of synoviocytes (H/E 10×). (f) Bursa: fibrosis, necrosis, and calcifications (H/E 20×)
Fig. 4
The figure shows the positive cells (brown) after immunohistochemical stain for anti-p65 antibody on the margins of the rotator cuff tear
Summarizing, histopathological findings suggest that changes in collagen and proteoglycans types and amount, degenerative modifications, and chondrometaplasia lead tendons to weakness and predispose it to the tear; the bursal tissue may play a prominent role in the healing process; stem cell role has to be deeply investigated.
References
