Background: Shoulder stiffness is a disease manifested by pain, limited range of motion, and functional
disability. The inflammatory and fibrosis processes play a substantial role in the pathogenesis of shoulder
stiffness. The CB1 receptor has been recognized to mediate the processes of pathologic fibrosis. This study
investigated the role of the CB1 pathway in pathogenesis of rotator cuff lesions with shoulder stiffness.
Methods: All of the patients undergoing repair surgery for rotator cuff lesions were recruited and subcategorized
into subjects with and without shoulder stiffness. Reverse transcription-polymerase chain reaction
assay was used to evaluate the expression level of CB1 and interleukin 1β (IL-1β) in the subacromial bursae,
and enzyme-linked immunosorbent assay was used to measure the concentration of CB1 and IL-1β in the
subacromial fluid. Tenocytes treated with CB1 agonists and antagonists were also studied for the relationship
of CB1 and the inflammatory cytokine IL-1β.
Results: The patients with shoulder stiffness had higher messenger RNA (mRNA) expression (P = .040)
and immunohistochemistry staining (P < .001) of CB1 in the subacromial bursa and higher CB1 concentration
in the subacromial fluid (P = .008). Tenocytes treated with the CB1 agonist WIN 55,212-2 and antagonist
AM251 showed increased expression of IL-1β mRNA (P = .049) and suppressed expression of IL-1β mRNA
(P = .001), respectively.