The senior population in India has been continuously growing, with those 65 and older estimated to account for 17% of the population by 2030. This rising population has its own set of health demands, and to satisfy them, a deeper knowledge of the physiological changes that occur as people age is required. The skeletal system goes through physiologic changes as we become older. Osteoporosis and osteoarthritis become more common as people get older. Furthermore, numerous studies show a higher rate of bone fracture, which is linked to increased morbidity and death. In this age, there is a decrease in healing potential, which can lead to a higher likelihood of delayed healing or nonunions. In the aged, delayed healing and the accompanying incapacitation might have more serious and systemic repercussions, posing particular issues for treating clinicians. While greater age has been linked to a variety of physiological changes, the mechanisms that lead to a reduction in fracture healing capacity are yet unknown.
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The lack of a thorough understanding of fracture healing in healthy and young people makes it difficult to grasp the age-related impacts on fracture healing. However, we can examine disparities in fracture healing between young and old humans by evaluating the specific components of fracture healing that we do understand.
Bone Fracture Healing Physiology
Fracture healing is divided into several stages, each with its own set of anabolic and catabolic processes. The early stages of healing are characterized by a robust inflammatory response that is responsible for debriding the fracture site and contributing to the signaling milieu that will propagate the subsequent stages of healing, including skeletal tissue progenitor cell recruitment and differentiation. After the initial inflammatory response, the anabolic phase begins. A soft callus with a central cartilaginous zone and fresh bone growth at the periphery is formed by progenitor cells. Avascular cartilage tissue that produces vascularization characterizes the soft callus. A hard callus forms as a result of endochondral ossification, which includes enhanced mineralization and the transdifferentiation of chondrocytes into osteoblasts. Finally, catabolic mechanisms are involved in callus remodeling. The callus shrinks, and osteoblastic and osteoclastic processes alternate to restore the normal hematopoietic and trabecular structure, returning the bone to its pre-injury form.
Fracture Healing and Inflammation
A strong inflammatory response characterizes the early stages of fracture healing. Pro-inflammatory cytokines must be secreted at this time to start the healing process and ensure proper recovery. For optimal bone fracture healing, temporal management of the inflammatory response is critical. Inflammation must be addressed after the initial pro-inflammatory phase for anabolic processes to begin and sustain the subsequent healing phases. However, as people become older, their immune systems change, and persistent inflammation and/or a reduced ability to resolve inflammatory processes can have a deleterious impact on bone fracture repair.
Immunosenescence and Inflamm-Aging
Inflamm-aging can also be caused by changes in the immune system as people get older. Immunosenescence is the term used to characterize the aging of the adaptive immune response. Immunosenescence is a term used to describe a decline of immunological function in the aged that is linked to an increased risk of infection and disease. Changes in T and B cell production and maturation are linked to increasing age. Age-related alterations to the bone marrow hematopoietic compartment and the thymus have a deleterious impact on T cell generation and maturation.
Cellular Regulation of Inflammation
Understanding the intrinsic age-related alterations in cells involved in the inflammatory response may help to explain why the elderly have a lower healing capability. Local cells of the innate and adaptive immune systems help to regulate the inflammatory response at the fracture site. Macrophages are potent anti-inflammatory regulators. Macrophages are classically activated and show an M1 phenotype during the early inflammatory stage of healing.
Fracture Healing and Vasculature
Adequate vascularization of the tissue is required for successful bone fracture repair. The vasculature plays a role in fracture healing by supplying blood for the transfer of nutrients and cells, as well as endothelial cells that express angiogenic and osteogenic signaling molecules locally and deliver oxygen to the healing callus.
Throughout the various stages of bone fracture healing, increasing age has been demonstrated to have a deleterious impact on cellular and molecular processes. Age-related alterations have an impact on inflammatory control, cellular differentiation, and signaling cascades. Our current understanding of these age-related alterations only partially explains the lower healing ability and higher complications seen in senior patients during fracture repair. To allow treatments to target specific age-related weaknesses and provide better care for the growing geriatric population, a greater understanding is required.