Charles J Mann1, Anne M Bradley2, Eleanor R Jones3, Iain R McNamara4, Toby O Smith5, Graham P Riley3. 1. Department of Trauma and Orthopaedics Norfolk and Norwich University NHS Foundation Trust, Colney Lane, Norwich NR4 7UY, United Kingdom of Great Britain and Northern Ireland; Faculty of Medicine and Health Sciences, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, United Kingdom of Great Britain and Northern Ireland. Electronic address: charles.mann@nnuh.nhs.uk. 2. Department of Trauma and Orthopaedics Norfolk and Norwich University NHS Foundation Trust, Colney Lane, Norwich NR4 7UY, United Kingdom of Great Britain and Northern Ireland. 3. School of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, United Kingdom of Great Britain and Northern Ireland. 4. Department of Trauma and Orthopaedics Norfolk and Norwich University NHS Foundation Trust, Colney Lane, Norwich NR4 7UY, United Kingdom of Great Britain and Northern Ireland; Faculty of Medicine and Health Sciences, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, United Kingdom of Great Britain and Northern Ireland. 5. Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Botnar Research Centre, Oxford OX3 7LD, United Kingdom of Great Britain and Northern Ireland.
Abstract
BACKGROUND: To establish proof of principle of a link between phenotypic expression and stiffness after TKR. METHODS: From 100 patients, genetic expression of markers of fibrosis was performed for 15 synovial samples from patients categorised as 'best post-operative range of movement (ROM)' and 15 samples from patients with 'worst ROM'. These markers included Matrix Metalloproteinases (MMPs), A Disintegrin and Metalloproteinases with Thrombospondin (ADAMTS) and Tissue Inhibitors of Matrix Metalloproteinases (TIMPs). Genetic marker data were compared to Oxford Knee Scores (OKS) and Pain Catastrophizing Scores (PCS). RESULTS: Quantitative markers for gene expression demonstrated more outliers in stiff compared to non-stiff knees, suggesting a greater imbalance in pro- and anti-fibrotic markers in stiff knees. Whilst there was a significant difference in the range of post-operative knee flexion (p = 0.001) and extension (p = 0.001), there was no statistically significant difference between stiff and non-stiff knees in pre-operative or post-operative OKS (p ≥ 0.06). There was no difference in the individual components of the individual PCS score items nor the PCS total scores when stiff and non-stiff knees were compared (p > 0.05). CONCLUSION: Biological factors, namely gene expression of MMPs, TIMPs and ADAMTS, may contribute towards post-TKR stiffness. This now warrants further investigation to better understand this relationship based on larger, multi-centre, cohorts. LEVEL OF EVIDENCE: Level 3. Crown
BACKGROUND: To establish proof of principle of a link between phenotypic expression and stiffness after TKR. METHODS: From 100 patients, genetic expression of markers of fibrosis was performed for 15 synovial samples from patients categorised as 'best post-operative range of movement (ROM)' and 15 samples from patients with 'worst ROM'. These markers included Matrix Metalloproteinases (MMPs), A Disintegrin and Metalloproteinases with Thrombospondin (ADAMTS) and Tissue Inhibitors of Matrix Metalloproteinases (TIMPs). Genetic marker data were compared to Oxford Knee Scores (OKS) and Pain Catastrophizing Scores (PCS). RESULTS: Quantitative markers for gene expression demonstrated more outliers in stiff compared to non-stiff knees, suggesting a greater imbalance in pro- and anti-fibrotic markers in stiff knees. Whilst there was a significant difference in the range of post-operative knee flexion (p = 0.001) and extension (p = 0.001), there was no statistically significant difference between stiff and non-stiff knees in pre-operative or post-operative OKS (p ≥ 0.06). There was no difference in the individual components of the individual PCS score items nor the PCS total scores when stiff and non-stiff knees were compared (p > 0.05). CONCLUSION: Biological factors, namely gene expression of MMPs, TIMPs and ADAMTS, may contribute towards post-TKR stiffness. This now warrants further investigation to better understand this relationship based on larger, multi-centre, cohorts. LEVEL OF EVIDENCE: Level 3. Crown