A bone fracture is a break in the continuity of the bone structure, triggering a highly coordinated biological response. Unlike soft tissue healing, which often results in a scar, bone healing is a regenerative process designed to restore the bone’s original structure, strength, and function. This complex repair mechanism unfolds in a predictable sequence of overlapping biological phases.
The Inflammatory Phase and Hematoma Formation
The inflammatory phase is the first stage in bone fracture healing, beginning seconds after injury and lasting several days, typically peaking within 48 to 72 hours. Trauma causes blood vessels in the bone and surrounding tissues to rupture, leading to internal bleeding. This pooled blood quickly clots, forming a fracture hematoma that envelops the fracture ends.
The hematoma acts as a scaffold for subsequent tissue formation and provides growth factors and signaling molecules. Specialized immune cells, such as neutrophils and macrophages, are recruited to initiate an intense inflammatory reaction, clearing away dead bone fragments and cellular debris.
These inflammatory cells release chemical mediators, including cytokines and growth factors, that signal the body to begin repair. These signals attract mesenchymal stem cells (MSCs) from the periosteum and bone marrow, preparing them to differentiate into new tissue. Swelling, pain, and redness characterize this phase, reflecting the internal cleanup process.
Soft Callus Formation
Soft callus formation begins as acute inflammation subsides, typically around one week after injury. The fracture hematoma is infiltrated by new capillaries and fibroblasts, forming highly vascularized granulation tissue. Mesenchymal stem cells differentiate into chondroblasts and fibroblasts, which deposit an extracellular matrix rich in collagen and cartilage.
This creates a soft, non-mineralized matrix composed of fibrocartilage that bridges the gap between the bone fragments. This fibrocartilaginous callus provides the first measure of biological stability, though it remains soft and flexible. The soft callus acts as a provisional splint, holding the bone ends in alignment but offering minimal resistance against bending forces.
Hard Callus Formation
The next stage involves hardening and strengthening this temporary structure through ossification. Osteoblasts, the primary bone-forming cells, migrate into the soft callus and deposit mineral salts, primarily calcium phosphate, onto the fibrocartilage matrix. This process is known as endochondral ossification, where cartilage is systematically replaced by bone tissue.
The soft tissue converts into a hard callus composed of woven bone, an immature form of bone. This bony callus provides significantly greater structural support and mechanical rigidity, marking “clinical union” where the fracture site can withstand external forces. The hard callus often appears as a noticeable, bulbous enlargement around the fracture site on an X-ray. This phase starts a few weeks post-injury and lasts several months until the fracture is mechanically stable.
Bone Remodeling
Bone remodeling is the final and longest phase of fracture healing, beginning once the hard callus has formed and continuing for months or even years. The purpose of this stage is to refine and reshape the temporary, bulky woven bone back into mature, compact bone with its original architectural strength. This process relies on the coordinated activity of two specialized cell types: osteoclasts and osteoblasts.
Osteoclasts are bone-resorbing cells that systematically remove the excess woven bone of the callus. Simultaneously, osteoblasts lay down new, stronger lamellar bone organized into the characteristic structure of normal bone tissue. The reshaping is guided by mechanical stress and weight-bearing forces applied to the bone, a principle known as Wolff’s Law.