 Hip osteoarthritis is a degenerative and painful disorder. The disease affects an estimated 21% of the population between the ages of 45 and 54, and twice that fraction among people over 75. Nearly half of cases of hip osteoarthritis can be traced to femoral acetabular impingement, the growth of extra bone over the hip joint. The progression from impingement to osteoarthritis is believed to be mediated by the release of inflammatory molecules across the hip cartilage, but the exact mechanisms are unknown. To address this gap, researchers tracked levels and patterns of inflammatory markers and cartilage from patients with symptoms of impingement. Their findings highlight the role of inflammation in upsetting joint homeostasis. The research team examined full thickness cartilage samples gathered from the zone of impingement in 45 patients undergoing hip surgery. Reasons for surgery fell into one of three groups, early disease, late disease or hip dysplasia. Early disease referred to symptomatic CAM impingement, which describes the overgrowth of bone across the femoral head, whereas late disease was defined as advanced osteoarthritis secondary to CAM impingement. Patients undergoing treatment for hip dysplasia were included for comparison, as dysplasia represents a degradation mechanism different from that of impingement. Samples from seven young adult donors served as controls. Early or late disease cartilage showed worse degenerative changes than cartilage from hips with dysplasia. These included poorer structure, lower cell counts, lower amounts of cartilage supporting proteins, and a blurring of the normally distinct boundary between hard and soft cartilage. The variation suggested that impingement elicits an inflammatory response in articular cartilage. To find out, the team then examined the expression of inflammatory molecules in the different samples. The two groups of hips showing signs of impingement exhibited unique patterns of inflammation. Compared with hips with dysplasia and control hips, they expressed higher concentrations of inflammatory and degradative proteins, such as interleukin 1 beta, acytokine involved in osteoarthritis, matrix metalloprotonase 13, an enzyme linked to tissue remodeling, and atoms 4, an enzyme associated with cartilage degradation in osteoarthritis. To be sure, hips with dysplasia did express the same molecules, but their expression was confined to the superficial zone of cartilage. In hips with impingement, these molecules were expressed in all cartilage zones. This more extensive pattern suggests that inflammation due to impingement results from chronic shear stress. Overall, these findings hint at the possibility that molecular inflammation in the hip could be a mechanism that links CAM impingement to osteoarthritis. Further clinical and translational studies are needed to determine whether and how surgical treatment could improve joint health in patients with hip impingement.