What is fracture?

A fracture, commonly known as a broken bone, occurs when there is a disruption or crack in the continuity of a bone. Fractures can range in severity from minor cracks or hairline fractures to complete breaks where the bone is separated into two or more pieces. Fractures can occur in any bone in the body, and they can result from various causes, including trauma, falls, direct blows, overuse, or underlying medical conditions that weaken the bones.


There are several types of fractures, each with its own characteristics:


  • Closed (Simple) Fracture: In a closed fracture, the bone breaks without piercing the skin. The skin remains intact, and there is no external wound at the site of the fracture.


  • Open (Compound) Fracture: In an open fracture, the broken bone penetrates through the skin, leading to an open wound. Open fractures are at higher risk of infection due to exposure to external contaminants.


  • Complete Fracture: A complete fracture occurs when the bone is completely broken into two or more separate pieces.


  • Incomplete Fracture: An incomplete fracture, also known as a hairline fracture or greenstick fracture, occurs when the bone is partially cracked or bent but not completely broken. This type of fracture is more common in children, whose bones are more flexible.


  • Displaced Fracture: In a displaced fracture, the bone fragments are out of alignment or displaced from their normal position. This can result in deformity and may require manipulation to realign the bones for proper healing.


  • Non-displaced Fracture: In a non-displaced fracture, the bone fragments remain in their normal alignment, with no significant displacement. Non-displaced fractures are often stable and may require less aggressive treatment.


  • Comminuted Fracture: A comminuted fracture occurs when the bone is broken into multiple fragments or pieces. This type of fracture may result from high-energy trauma or crushing injuries.


  • Pathological Fracture: A pathological fracture occurs when the bone is weakened by an underlying medical condition, such as osteoporosis, cancer, or infection. These fractures may occur with minimal trauma or even with normal activities.


What is the relationship between fracture and oxidative stress?

The relationship between fractures and oxidative stress is complex and multifaceted, involving various mechanisms related to the inflammatory response, tissue damage, and repair processes following a bone injury. Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, leading to cellular damage and dysfunction. Several factors contribute to oxidative stress following a fracture:


  • Inflammatory Response: Fractures trigger an inflammatory response, characterized by the recruitment of immune cells, release of pro-inflammatory cytokines, and activation of inflammatory pathways. Inflammatory cells such as neutrophils and macrophages produce ROS as part of their antimicrobial defense mechanisms to eliminate pathogens and promote tissue repair. However, excessive ROS production during inflammation can lead to oxidative stress and tissue damage, prolonging the inflammatory phase of fracture healing.


  • Ischemia-Reperfusion Injury: Fractures disrupt blood vessels and reduce blood flow to the injured area, leading to tissue ischemia (lack of oxygen) and subsequent reperfusion injury when blood flow is restored. Ischemia-reperfusion injury results in the production of ROS, which can cause oxidative damage to tissues and exacerbate inflammation. ROS generated during ischemia-reperfusion contribute to oxidative stress and impair fracture healing.


  • Tissue Damage and Repair Processes: Fractures cause mechanical trauma and tissue damage to the bone and surrounding soft tissues. The repair processes following a fracture, including inflammation, angiogenesis (formation of new blood vessels), and bone remodeling, require the generation of ROS as signaling molecules to regulate cell proliferation, differentiation, and matrix synthesis. However, excessive ROS production can overwhelm the antioxidant defenses and lead to oxidative stress, inhibiting the normal healing response and delaying fracture healing.


  • Bone Remodeling: Fracture healing involves a complex series of events, including inflammation, callus formation, bone resorption, and new bone formation. ROS play a role in bone remodeling by regulating osteoclast and osteoblast activity, which are responsible for bone resorption and formation, respectively. Imbalance between ROS production and antioxidant defenses can disrupt the delicate balance of bone remodeling, leading to impaired fracture healing and delayed bone union.


  • Underlying Conditions: Underlying medical conditions such as diabetes mellitus, osteoporosis, and aging can exacerbate oxidative stress and impair fracture healing. Diabetes and osteoporosis are associated with chronic inflammation, impaired antioxidant defenses, and increased oxidative stress, which can compromise fracture healing. Aging is also associated with reduced antioxidant capacity and increased susceptibility to oxidative damage, leading to impaired fracture healing in older individuals.


Overall, oxidative stress plays a significant role in the pathogenesis and progression of fractures by exacerbating inflammation, impairing tissue repair processes, and disrupting bone remodeling.