Cameron J Elias-Jones1, Luke Farrow2, James H Reilly2, Shauna Kerr2, R M Dominic Meek3, Michael P Kelly4, J Luke Campton4, Neal L Millar5. 1. Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK Department of Orthopaedic Surgery, Southern General Hospital, Glasgow, UK. 2. Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK. 3. Department of Orthopaedic Surgery, Southern General Hospital, Glasgow, UK. 4. Department of Orthopaedic Surgery, Western Infirmary, Glasgow, UK. 5. Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK Department of Orthopaedic Surgery, Western Infirmary, Glasgow, UK neal.millar@glasgow.ac.uk.
Abstract
BACKGROUND: Femoroacetabular impingement (FAI) is a significant cause of osteoarthritis (OA) in young active patients, but the pathophysiology remains unclear. Increasingly, mechanistic studies point toward an inflammatory component in OA. PURPOSE: This study aimed to characterize inflammatory cell subtypes and neovascularization in FAI by exploring the phenotype and quantification of inflammatory cells and neovascularization in FAI versus OA samples. STUDY DESIGN: Descriptive laboratory study. METHODS: Ten samples of the labrum were obtained from patients with FAI (confirmed diagnosis) during open osteochondroplasty or hip arthroscopic surgery. Control samples of the labrum were collected from 10 patients with OA who were undergoing total hip arthroplasty. Labral biopsy specimens were evaluated immunohistochemically by quantifying the presence of macrophages (CD68, CD206, interleukin-13 [IL-13]), T cells (CD3), mast cells (mast cell tryptase), and vascular endothelium (CD34, vascular endothelial growth factor). RESULTS: Labral biopsy specimens obtained from patients with FAI exhibited significantly greater macrophage, mast cell, and vascular endothelium expression compared with control OA labral samples (P < .05). The most significant difference was noted in macrophage (P < .01) and mast cell (P < .05) expression. Further subtyping of macrophages in FAI using the CD206 tissue marker and IL-13 revealed an M2 phenotype, suggesting that these cells are involved in a regenerate versus degenerate process. There was a modest but significant correlation between mast cells and CD34 expression (r = 0.4, P < .01) in FAI samples. CONCLUSION: This study provides evidence for an inflammatory cell infiltrate in FAI along with significant neovascularization. In particular, the significant infiltration of mast cells and macrophages was demonstrated, suggesting a role for innate immune pathways in the events that mediate hip impingement. CLINICAL RELEVANCE: Further mechanistic studies to evaluate the net contribution and hence therapeutic utility of these cellular lineages and their downstream processes may reveal novel therapeutic approaches to the management of early hip impingement.
BACKGROUND: Femoroacetabular impingement (FAI) is a significant cause of osteoarthritis (OA) in young active patients, but the pathophysiology remains unclear. Increasingly, mechanistic studies point toward an inflammatory component in OA. PURPOSE: This study aimed to characterize inflammatory cell subtypes and neovascularization in FAI by exploring the phenotype and quantification of inflammatory cells and neovascularization in FAI versus OA samples. STUDY DESIGN: Descriptive laboratory study. METHODS: Ten samples of the labrum were obtained from patients with FAI (confirmed diagnosis) during open osteochondroplasty or hip arthroscopic surgery. Control samples of the labrum were collected from 10 patients with OA who were undergoing total hip arthroplasty. Labral biopsy specimens were evaluated immunohistochemically by quantifying the presence of macrophages (CD68, CD206, interleukin-13 [IL-13]), T cells (CD3), mast cells (mast cell tryptase), and vascular endothelium (CD34, vascular endothelial growth factor). RESULTS: Labral biopsy specimens obtained from patients with FAI exhibited significantly greater macrophage, mast cell, and vascular endothelium expression compared with control OA labral samples (P < .05). The most significant difference was noted in macrophage (P < .01) and mast cell (P < .05) expression. Further subtyping of macrophages in FAI using the CD206 tissue marker and IL-13 revealed an M2 phenotype, suggesting that these cells are involved in a regenerate versus degenerate process. There was a modest but significant correlation between mast cells and CD34 expression (r = 0.4, P < .01) in FAI samples. CONCLUSION: This study provides evidence for an inflammatory cell infiltrate in FAI along with significant neovascularization. In particular, the significant infiltration of mast cells and macrophages was demonstrated, suggesting a role for innate immune pathways in the events that mediate hip impingement. CLINICAL RELEVANCE: Further mechanistic studies to evaluate the net contribution and hence therapeutic utility of these cellular lineages and their downstream processes may reveal novel therapeutic approaches to the management of early hip impingement.
Authors: Leandro Ejnisman; Benjamin G Domb; Felipe Souza; Consuelo Junqueira; Jose Ricardo Negreiros Vicente; Alberto Tesconi Croci Journal: PLoS One Date: 2018-06-21 Impact factor: 3.240
Authors: Masahiko Haneda; Muhammad Farooq Rai; Lei Cai; Robert H Brophy; Regis J O'Keefe; John C Clohisy; Cecilia Pascual-Garrido Journal: Am J Sports Med Date: 2020-08 Impact factor: 6.202