What Is a Pathologic Fracture and What Causes It?

A pathologic fracture is a break in a bone caused by an underlying disease process, rather than by a significant force or injury. This type of fracture occurs because the bone tissue has been structurally compromised and weakened before the injury takes place. The break happens with minimal trauma, often from a simple movement or a low-energy fall that a healthy bone would easily withstand.

How Pathologic Fractures Differ From Traumatic Breaks

The defining difference between a pathologic fracture and a traumatic break lies in the amount of mechanical energy required to cause the injury. A typical traumatic fracture, such as one sustained in a car accident or a high-impact fall, involves a high-energy force overwhelming the structural integrity of a normal, healthy bone. The bone itself is sound before the incident.

In contrast, a pathologic fracture occurs when the bone’s architecture is already compromised by a disease, making it fragile. The force that causes the break is often minimal, such as stepping off a curb, coughing, or simply bearing normal weight. The bone fails because its internal strength has been reduced to a point where it can no longer support routine daily stresses.

Underlying Conditions That Weaken Bone Structure

A variety of diseases can weaken bone sufficiently to result in a pathologic fracture, with malignant conditions being a primary concern. Metastatic cancer is the most common cause in adults, occurring when cancer cells from a primary tumor spread to the bone. Cancers originating in the breast, lung, prostate, kidney, and thyroid are the most frequent sources of these bone metastases. These cancerous lesions destroy or replace the normal bone matrix, creating lytic (bone-destroying) or mixed lesions that act as weak points.

Primary bone tumors, which originate directly in the bone tissue, also compromise structural integrity, though they are much less common than metastatic disease. Examples include osteosarcoma and multiple myeloma, which causes widespread bone destruction and thinning. The presence of these abnormal cells disrupts the balance of bone remodeling, leading to a loss of strength.

Beyond malignant diseases, several non-malignant conditions can predispose a person to pathologic fractures. Osteoporosis, characterized by low bone mass and deterioration of bone tissue, creates generalized skeletal fragility. This metabolic disorder often leads to insufficiency fractures, particularly in the spine and hip, from minimal force.

Metabolic bone diseases, such as Paget’s disease, cause abnormal bone remodeling, resulting in disorganized and weakened bone areas. Osteomalacia involves defective mineralization of bone tissue, making the skeleton soft and vulnerable to breaking. Infections of the bone, known as osteomyelitis, can also weaken the structure by causing localized bone destruction and abscess formation.

Identifying Pathologic Fractures and Their Source

The diagnostic process must accomplish two goals: confirming the presence of the break and determining the specific underlying disease. Initial imaging often begins with plain X-rays, which reveal not only the fracture line but also the unusual nature of the bone surrounding the break. These images may show a destructive lesion, bone thinning, or evidence of a tumor mass.

To characterize the extent of bone destruction and soft tissue involvement, advanced imaging techniques are employed. Computed Tomography (CT) scans provide detailed cross-sectional views of the bone structure. Magnetic Resonance Imaging (MRI) is superior for visualizing soft tissues, bone marrow, and any tumor mass. These images help surgeons plan for stabilization and guide biopsy procedures.

Identifying the root cause requires laboratory work and often a biopsy. Blood tests check for abnormalities that can point toward a specific disease, such as elevated serum calcium and alkaline phosphatase levels, or specific tumor markers like prostate-specific antigen (PSA). Serum or urine protein electrophoresis may be used to screen for conditions like multiple myeloma.

A biopsy, which involves taking a small tissue sample from the abnormal bone area, is necessary to obtain a definitive diagnosis. This microscopic analysis confirms whether the lesion is malignant, benign, infectious, or metabolic, allowing for precise classification and guiding the treatment plan.

Managing the Fracture and the Root Cause

The management of a pathologic fracture is dual-focused, requiring immediate orthopedic stabilization of the broken bone while simultaneously addressing the disease that caused the weakness. Because the underlying disease compromises the bone’s natural ability to heal, surgical intervention is required to provide lasting stability. Stabilization may involve placing internal fixation devices, such as rods, plates, or screws, to secure the fracture site and prevent collapse.

In cases involving the spine, procedures like vertebroplasty or kyphoplasty may be performed to inject bone cement into the fractured vertebra, providing immediate pain relief and mechanical support. The goal of fracture management is to restore mechanical function and allow the patient to mobilize quickly, even if the bone itself will never fully heal due to the disease.

Treating the underlying condition is paramount for preventing further fractures in other parts of the skeleton. For fractures caused by cancer, therapies such as targeted chemotherapy, external beam radiation therapy, or hormonal treatments are used to shrink or eliminate the tumor. Radiation is effective at treating painful bone metastases and promoting localized bone healing.

In non-malignant cases, the root cause is managed with specific medical interventions. Bone-strengthening medications, like bisphosphonates or denosumab, are administered to treat osteoporosis and reduce the risk of future insufficiency fractures. Infections like osteomyelitis require prolonged courses of targeted antibiotics, often delivered intravenously, to eradicate the bacterial or fungal presence.