Dan Clark1,2,3, Mary Nakamura4,5, Ted Miclau1,2, Ralph Marcucio6,7. 1. Department of Orthopaedic Surgery, University of California at San Francisco, 513 Parnassus Ave., San Francisco, CA, 94143, USA. 2. Orthopaedic Trauma Institute, Zuckerberg San Francisco General Hospital and Trauma Center, 2550 23rd St, Building 9, San Francisco, CA, 94110, USA. 3. Department of Oral and Craniofacial Sciences, School of Dentistry, University of California at San Francisco, 513 Parnassus Ave., Rm. S-619A, San Francisco, CA, 94143, USA. 4. Department of Medicine, University of California at San Francisco, San Francisco, CA, 94143-0451, USA. 5. Department of Pathology, VA Medical Center, University of California San Francisco & Pathology Service, San Francisco, CA, 94121, USA. 6. Department of Orthopaedic Surgery, University of California at San Francisco, 513 Parnassus Ave., San Francisco, CA, 94143, USA. Ralph.marcucio@ucsf.edu. 7. Orthopaedic Trauma Institute, Zuckerberg San Francisco General Hospital and Trauma Center, 2550 23rd St, Building 9, San Francisco, CA, 94110, USA. Ralph.marcucio@ucsf.edu.
Abstract
PURPOSE OF REVIEW: This review summarizes research on the physiological changes that occur with aging and the resulting effects on fracture healing. RECENT FINDINGS: Aging affects the inflammatory response during fracture healing through senescence of the immune response and increased systemic pro-inflammatory status. Important cells of the inflammatory response, macrophages, T cells, mesenchymal stem cells, have demonstrated intrinsic age-related changes that could impact fracture healing. Additionally, vascularization and angiogenesis are impaired in fracture healing of the elderly. Finally, osteochondral cells and their progenitors demonstrate decreased activity and quantity within the callus. Age-related changes affect many of the biologic processes involved in fracture healing. However, the contributions of such changes do not fully explain the poorer healing outcomes and increased morbidity reported in elderly patients. Future research should address this gap in understanding in order to provide improved and more directed treatment options for the elderly population.
PURPOSE OF REVIEW: This review summarizes research on the physiological changes that occur with aging and the resulting effects on fracture healing. RECENT FINDINGS: Aging affects the inflammatory response during fracture healing through senescence of the immune response and increased systemic pro-inflammatory status. Important cells of the inflammatory response, macrophages, T cells, mesenchymal stem cells, have demonstrated intrinsic age-related changes that could impact fracture healing. Additionally, vascularization and angiogenesis are impaired in fracture healing of the elderly. Finally, osteochondral cells and their progenitors demonstrate decreased activity and quantity within the callus. Age-related changes affect many of the biologic processes involved in fracture healing. However, the contributions of such changes do not fully explain the poorer healing outcomes and increased morbidity reported in elderly patients. Future research should address this gap in understanding in order to provide improved and more directed treatment options for the elderly population.
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