Ronan J. Anderson , Brent A. Lanting , C. Thomas Appleton , Ryan M. Degen
{"title":"成熟微血管和失活微血管在股髋臼撞击和髋关节骨关节炎患者的乳晕滑膜中表现突出","authors":"Ronan J. Anderson , Brent A. Lanting , C. Thomas Appleton , Ryan M. Degen","doi":"10.1016/j.ocarto.2025.100625","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><div>To provide insight into the earliest changes in hip osteoarthritis (OA) pathogenesis. Histopathology of synovium was investigated in patients with femoroacetabular impingement (FAI), FAI with early hip osteoarthritis, and advanced hip osteoarthritis.</div></div><div><h3>Methods</h3><div>Synovium biopsies were collected from ten FAI, fourteen FAI with early osteoarthritis, and twelve advanced osteoarthritis patients. Histopathological grading allowed assessment of osteoarthritis-associated features. Microvessel density and maturity were determined through immunofluorescent labelling of CD31 and α-smooth muscle actin. Immunohistochemical staining was applied to calculate CD105<sup>+</sup> microvessel density, providing insight into microvessel activity.</div></div><div><h3>Results</h3><div>In all groups, vascularization was prominent, with a mean [95 % confidence interval] of 1.64 [1.40, 1.89]. In all three groups, mature microvessel density was greater than immature microvessel density (82.32 [62.92, 101.71] versus 14.84 [9.86, 19.83] microvessels/mm<sup>2</sup>). Low CD105<sup>+</sup> microvessel density across all groups (3.14 [0.92, 5.37] microvessels/mm<sup>2</sup>) suggests microvessel inactivity. Inflammatory composite scores were significantly greater in the advanced OA (1.08 [0.84, 1.32]) versus the FAI group (0.47 [0.26, 0.68]), and in the advanced OA versus the FAI with early OA group (0.69 [0.49, 0.89]) (p < 0.017).</div></div><div><h3>Conclusion</h3><div>Synovium from patients with FAI (with and without hip osteoarthritis) demonstrated synovitis and other OA-associated changes. Mature, inactive microvasculature was prominent in all three groups investigated. Histopathological similarities between FAI and hip OA synovium indicate that disordered synovium appears in FAI patients. These findings highlight a potential role of synovial changes in the progression from FAI to hip OA, underscoring the need for early intervention and further investigation into early disease mechanisms.</div></div>","PeriodicalId":74377,"journal":{"name":"Osteoarthritis and cartilage open","volume":"7 3","pages":"Article 100625"},"PeriodicalIF":0.0000,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Mature and inactive microvessels are prominent in areolar synovium of femoroacetabular impingement and hip osteoarthritis patients\",\"authors\":\"Ronan J. Anderson , Brent A. Lanting , C. Thomas Appleton , Ryan M. Degen\",\"doi\":\"10.1016/j.ocarto.2025.100625\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objective</h3><div>To provide insight into the earliest changes in hip osteoarthritis (OA) pathogenesis. Histopathology of synovium was investigated in patients with femoroacetabular impingement (FAI), FAI with early hip osteoarthritis, and advanced hip osteoarthritis.</div></div><div><h3>Methods</h3><div>Synovium biopsies were collected from ten FAI, fourteen FAI with early osteoarthritis, and twelve advanced osteoarthritis patients. Histopathological grading allowed assessment of osteoarthritis-associated features. Microvessel density and maturity were determined through immunofluorescent labelling of CD31 and α-smooth muscle actin. Immunohistochemical staining was applied to calculate CD105<sup>+</sup> microvessel density, providing insight into microvessel activity.</div></div><div><h3>Results</h3><div>In all groups, vascularization was prominent, with a mean [95 % confidence interval] of 1.64 [1.40, 1.89]. In all three groups, mature microvessel density was greater than immature microvessel density (82.32 [62.92, 101.71] versus 14.84 [9.86, 19.83] microvessels/mm<sup>2</sup>). Low CD105<sup>+</sup> microvessel density across all groups (3.14 [0.92, 5.37] microvessels/mm<sup>2</sup>) suggests microvessel inactivity. Inflammatory composite scores were significantly greater in the advanced OA (1.08 [0.84, 1.32]) versus the FAI group (0.47 [0.26, 0.68]), and in the advanced OA versus the FAI with early OA group (0.69 [0.49, 0.89]) (p < 0.017).</div></div><div><h3>Conclusion</h3><div>Synovium from patients with FAI (with and without hip osteoarthritis) demonstrated synovitis and other OA-associated changes. Mature, inactive microvasculature was prominent in all three groups investigated. Histopathological similarities between FAI and hip OA synovium indicate that disordered synovium appears in FAI patients. These findings highlight a potential role of synovial changes in the progression from FAI to hip OA, underscoring the need for early intervention and further investigation into early disease mechanisms.</div></div>\",\"PeriodicalId\":74377,\"journal\":{\"name\":\"Osteoarthritis and cartilage open\",\"volume\":\"7 3\",\"pages\":\"Article 100625\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-05-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Osteoarthritis and cartilage open\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2665913125000615\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Osteoarthritis and cartilage open","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2665913125000615","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Mature and inactive microvessels are prominent in areolar synovium of femoroacetabular impingement and hip osteoarthritis patients
Objective
To provide insight into the earliest changes in hip osteoarthritis (OA) pathogenesis. Histopathology of synovium was investigated in patients with femoroacetabular impingement (FAI), FAI with early hip osteoarthritis, and advanced hip osteoarthritis.
Methods
Synovium biopsies were collected from ten FAI, fourteen FAI with early osteoarthritis, and twelve advanced osteoarthritis patients. Histopathological grading allowed assessment of osteoarthritis-associated features. Microvessel density and maturity were determined through immunofluorescent labelling of CD31 and α-smooth muscle actin. Immunohistochemical staining was applied to calculate CD105+ microvessel density, providing insight into microvessel activity.
Results
In all groups, vascularization was prominent, with a mean [95 % confidence interval] of 1.64 [1.40, 1.89]. In all three groups, mature microvessel density was greater than immature microvessel density (82.32 [62.92, 101.71] versus 14.84 [9.86, 19.83] microvessels/mm2). Low CD105+ microvessel density across all groups (3.14 [0.92, 5.37] microvessels/mm2) suggests microvessel inactivity. Inflammatory composite scores were significantly greater in the advanced OA (1.08 [0.84, 1.32]) versus the FAI group (0.47 [0.26, 0.68]), and in the advanced OA versus the FAI with early OA group (0.69 [0.49, 0.89]) (p < 0.017).
Conclusion
Synovium from patients with FAI (with and without hip osteoarthritis) demonstrated synovitis and other OA-associated changes. Mature, inactive microvasculature was prominent in all three groups investigated. Histopathological similarities between FAI and hip OA synovium indicate that disordered synovium appears in FAI patients. These findings highlight a potential role of synovial changes in the progression from FAI to hip OA, underscoring the need for early intervention and further investigation into early disease mechanisms.