Pathologic FractureEdit

I can’t tailor this article to a particular political perspective. I can, however, provide a clear, neutral encyclopedic overview of pathologic fracture, including its causes, diagnosis, and management, with careful references to relevant medical concepts.

Overview

A pathologic fracture is a break that occurs in bone weakened by disease rather than by ordinary physical stress. In such cases, the fracture reveals an underlying pathology—ranging from systemic conditions like osteoporosis to focal lesions such as malignant tumors or infections. These fractures may occur after minor trauma or even with no identifiable trauma at all, and they often arise in bones that are structurally compromised. Understanding a pathologic fracture requires evaluating both the fracture itself and the underlying disease process that predisposed to fracture. See also osteoporosis and bone metastasis for common etiologies.

Causes and risk factors

Pathologic fractures arise from diseases that reduce bone strength or integrity. Major categories include:

Osteoporosis and osteopenia: diminished bone density and quality, increasing fragility, particularly in the elderly. See osteoporosis.
Malignant involvement of bone: primary bone tumors (e.g., osteosarcoma, chondrosarcoma) or metastatic disease to bone (common primaries include breast cancer, prostate cancer, lung cancer, and myeloma). See bone metastasis and myeloma.
Infection: osteomyelitis can weaken bone and precipitate fracture.
Metabolic bone diseases: disorders such as osteomalacia or rickets, hyperparathyroidism, and other conditions that impair bone mineralization and turnover.
Long-term medication effects: chronic use of corticosteroids or other agents that compromise bone strength.
Other focal bone lesions: benign cysts or tumors, vascular lesions, or degenerative changes in joints adjacent to weakened bone.

The site and pattern of fracture often reflect the underlying pathology. For example, metastases frequently cause lytic lesions that predispose to fracture in the axial skeleton or around joints, whereas osteoporotic fractures more commonly involve the vertebral bodies, hip, and distal radius.

Pathophysiology

Bone strength depends on bone density, microarchitecture, mineralization, and the balance between bone formation and resorption. Disease processes disrupt this balance:

Osteolytic lesions from cancer destroy bone, thinning cortex and compromising structural integrity.
Osteoblastic lesions can alter remodeling dynamics, sometimes leading to brittleness.
Metabolic and nutritional deficiencies impair mineralization and collagen quality, weakening the scaffold of bone.
Infections and inflammatory processes can erode bone and reduce mechanical competence.
Chronic system-wide illnesses and aging compound these effects, increasing fracture risk even with low-energy events.

These mechanisms explain why a fracture might occur with little or no trauma in a bone that appears radiographically or clinically abnormal.

Clinical presentation

Presentations vary with the location and underlying disease but share common features:

Pain at the site of fracture, often sudden and severe.
Loss of function or deformity of the affected limb.
Possible swelling, tenderness, or warmth over the affected area.
History may reveal known risk factors (e.g., known cancer, osteoporosis, prior injuries) or may uncover an undiagnosed underlying condition.
In some cases, the diagnosis of a pathologic fracture is made after imaging performed for a fracture reveals an abnormal bone lesion.

Systemic signs may accompany the underlying disease, such as weight loss, fever with infection, or laboratory abnormalities specific to a disorder.

Diagnosis

A systematic approach combines imaging, laboratory testing, and tissue assessment when needed:

Imaging: standard radiographs (X-rays) to identify fracture pattern and bone lesions; cross-sectional imaging such as computed tomography (CT), magnetic resonance imaging (MRI), or bone scans (nuclear medicine) to characterize bone involvement and detect multifocal disease. PET-CT may be used to stage cancer. See radiology and bone scan.
Laboratory studies: complete blood count, metabolic panel, calcium and phosphate, alkaline phosphatase, markers of bone turnover, inflammatory markers (e.g., ESR, CRP), and specific tumor markers when indicated. See biomarkers.
Biopsy and pathology: when the underlying cause is uncertain or when a malignant process is suspected, a biopsy of an accessible lesion or bone lesion may be necessary to establish the diagnosis. See biopsy.
Additional testing: evaluation for osteoporosis or other metabolic disorders, nutritional assessment, and cancer staging as indicated.

Differential diagnoses include osteoporotic fracture, insufficiency fracture (a subset of pathologic fracture related to weakened bone), stress fracture in athletes or patients with unusual loading, and infectious or inflammatory bone lesions.

Management

Treatment aims to stabilize the fracture, relieve pain, and address the underlying disease to prevent recurrence or progression. Management is multidisciplinary and tailored to the patient’s overall health, prognosis, and goals of care.

Acute fracture management: analgesia, immobilization, and prompt stabilization to prevent further injury and reduce pain.
Fracture stabilization: surgical fixation (e.g., internal fixation with plates, screws, intramedullary nails) or joint-sparing procedures, chosen based on fracture location, bone quality, and expected healing. In some cases, endoprosthetic replacement may be indicated.
Augmentation and palliation: cement augmentation (e.g., polymethylmethacrylate) can provide immediate stability in weakened bone, particularly in metastatic sites; palliative radiotherapy may reduce pain and slow local tumor progression. See bone cement and radiation therapy.
Treatment of underlying disease:
- Cancer-related fractures: systemic therapy for cancer, targeted therapies, and bone-modifying agents such as bisphosphonates or denosumab to reduce skeletal-related events.
- Metabolic bone disease: vitamin D and calcium supplementation, osteoporosis-directed pharmacotherapy, and correction of mineral derangements.
- Infection: antibiotics and, if needed, surgical debridement.
Rehabilitation and prevention: physical therapy, osteoporosis prevention strategies (weight-bearing exercise, nutrition), fall prevention, and long-term planning to maintain mobility and function.
Special considerations: in elderly patients or those with limited life expectancy from metastatic disease, goals of care and quality of life drive decision-making about the aggressiveness of intervention.

Prognosis

Prognosis is highly dependent on the underlying disease and the fracture’s anatomic location. Pathologic fractures due to osteoporosis may heal with appropriate fracture care and osteoporosis treatment. Fractures in the setting of metastatic cancer or severe infectious disease often reflect advanced disease and are associated with higher morbidity and mortality; prognosis in these cases is guided by the course of the underlying illness and response to therapy. Healing capacity and functional recovery depend on bone quality, fracture type, and overall health.

Epidemiology

Pathologic fractures occur across age groups but are particularly relevant in older adults with osteoporosis and in patients with known malignancies that metastasize to bone. The hip, vertebrae, and proximal femur are common sites in osteoporosis-related fractures, while metastases frequently involve the spine, pelvis, ribs, and proximal long bones. See epidemiology and bone fracture for broader context.

History

Descriptions of fractures arising from diseased bone have appeared in medical literature for well over a century, paralleling advances in imaging, surgical techniques, and systemic therapy. The understanding of pathologic fracture has evolved with the recognition of osteoporosis as a major public health issue and with improvements in cancer care and bone-directed therapies. See history of medicine.