The early healing stage is characterized by a robust inflammatory response that is responsible for debriding the fracture site and contributing to the signaling milieu that will propagate the successive stages of healing, including recruitment and differentiation of skeletal tissue progenitor cells. Aged animals demonstrate decreased vascular density within the callus which is associated with decreased levels of key angiogenic factors required for healingįracture healing proceeds through multiple phases characterized by anabolic and catabolic processes. Finally, adequate vascularization is required for successful fracture healing. Aged macrophages demonstrate decreased proliferation and increased activation that may contribute to the poorer healing outcomes associated with aged macrophages compared to young. Macrophages are important regulators of inflammation during fracture healing. T-cells contribute to fracture healing and production and maturation of T cells is negatively affected by age-related changes to the bone marrow hematopoietic compartment and to the thymus. Osteochondral stem cells arise from the periosteum and bone marrow and demonstrate decreased quantity, increased oxidative damage, and decreased osteoblastic and chondrogenic differentiation potential with age. Stem cells and immune cells involved in fracture healing demonstrate age-related changes that may negatively affect fracture healing. The effect of age on the cellular contribution to fracture healing.
Figure 1 summarizes the effect of age on critical cells that contribute to fracture healing. Cellular, molecular, and genetic differences between young and old humans and animal models will be characterized to illustrate the current understanding of the effect of age on bone fracture healing. This review will highlight the phases of fracture healing and the respective physiologic changes that occur with age. However, by analyzing the individual facets of fracture healing that we do understand we can compare differences in fracture healing between the young and old humans and animals. While increased age has been generally associated with a wide range of physiological changes, the mechanisms that result in decreased capacity for fracture healing are not fully understood.Īn understanding of the age-related effects to fracture healing is complicated by a lack of a complete understanding of fracture healing in healthy and in young individuals. Delayed healing, and the resulting incapacitation, can have more severe and systemic consequences in the elderly, which poses unique challenges for the treating clinician. A decline in healing potential is observed in the elderly, and this may result in increased rates of delayed healing or nonunions.
Additionally, many reports demonstrate a higher rate of bone fracture, and these are associated with increased morbidity and mortality. Conditions such as osteoporosis and osteoarthritis increase with age. The skeletal system exhibits physiologic changes that occur with increasing age.
This growing population presents their own unique health needs, and in order to meet these needs a better understanding of the physiologic changes that occur with aging is necessary. The elderly population in the USA has been steadily increasing, and those aged 65 years old and older are expected to comprise 17% of the population by 2030.
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