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Pathologic fracture
Pathologic fracture
Pathologic fracture
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Pathologic fracture
Other namesInsufficiency fracture
Pathological fracture of the humerus in a patient with metastasis of renal cell carcinoma
SpecialtyRheumatology Edit this on Wikidata

A pathologic fracture is a bone fracture caused by weakness of the bone structure that leads to decrease mechanical resistance to normal mechanical loads.[1] This process is most commonly due to osteoporosis, but may also be due to other pathologies such as cancer, infection (such as osteomyelitis), inherited bone disorders, or a bone cyst. Only a small number of conditions are commonly responsible for pathological fractures, including osteoporosis, osteomalacia, Paget's disease, Osteitis, osteogenesis imperfecta, benign bone tumours and cysts, secondary malignant bone tumours and primary malignant bone tumours.

Fragility fracture is a type of pathologic fracture that occurs as a result of an injury that would be insufficient to cause fracture in a normal bone.[2] There are several fracture sites said to be typical of fragility fractures: vertebral fractures, fractures of the neck of the femur, pelvic fractures, proximal humeral fractures and Colles fracture of the wrist[3]. This definition arises because a normal human being ought to be able to fall from standing height without breaking any bones, and a fracture, therefore, suggests weakness of the skeleton.

Pathological fractures present as a chalkstick fracture in long bones, and appear as a transverse fractures nearly 90 degrees to the long axis of the bone. In a pathological compression fracture of a spinal vertebra fractures will commonly appear to collapse the entire body of vertebra.

Cause

[edit]

Pathologic fractures in children and adolescents can result from a diverse array of disorders namely; metabolic, endocrine, neoplastic, infectious, immunologic, and genetic skeletal dysplasias. [citation needed]

Juvenile osteoporosis

Miscellaneous causes

[edit]

Diagnosis

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The underlying cause of the pathological fracture should always be found, to guide the optimal treatment path. If the cause is unknown, a thorough workup should be performed, including laboratory tests and radiological examinations - often magnetic resonance imaging of the affected area as well as computed tomography of the chest, abdomen and pelvis (for staging or identifying a primary malignancy). Often, a biopsy from the fracture site is taken to obtain a histopathological or cytological diagnosis. A common method of initial biopsy is a Fine Needle Aspiration Cytology (FNAC)[5].

In circumstances where other pathologies are excluded (for example, cancer), postmenopausal women or men aged >50 years who present with a hip fracture after a low-energy fall can be diagnosed with osteoporosis irrespective of bone mineral density, and offered treatment. Diagnosis can also be made ff a previous fragility fracture of the pelvis, vertebra, wrist or proximal humerus is present in combination with osteopenia[3].

Management

[edit]

Once a fracture has occurred, intramedullary fixation is the usual surgical management for certain long bones, such as the femur, tibia, and fibula.[6] However, the method of fixation should depend on several factors; The fracture location, underlying cause, prognosis of the underlying cause and patient activity level. Fracture healing potential is also different for different malignancies, which needs to be taken into account. For example, if the patients' life expectancy is long, fixation needs to be stronger to account for reduced healing potential, which could be an argument for total replacement of the fractured area with a prosthesis instead of internal fixation (which is dependent on fracture healing). On the other hand, in case of a patient with poor prognosis or low activity level, a minimally invasive internal fixation could be enough to improve quality of life - in this case the patient is either not expected to survive long enough for the fixation to fail, or are not active enough for reduced healing potential to become a problem[7].

For pathological fractures in the setting of metastatic disease where there is a need for postoperative radiation, a carbon fiber implant may be preferred due to its radiolucency, allowing better visualization of the affected area on x-ray imaging.[8]

Several scoring systems exist to help in the evaluation of impending pathological fractures (where a pathological process has weakened the bone but not yet caused a fracture). The most commonly used are Mirel's score (for metastatic disease in long bones) and Harrington's score (for metastatic disease in the proximal femur) . For both instruments, a higher score means a higher risk of fracture, based on similar criteria; fracture location, patient symptoms, size of lesion, and type of lesion. Based on Mirel's score (if the score is more than 8), bone fixation should be done prophylactically. Fixation is done by internal fixation rather than conservatively, along with treatment of the underlying cause.[9][10]

References

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Pathologic fracture

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A pathologic fracture is a break in a that occurs due to underlying from disease or abnormality, rather than from significant trauma, distinguishing it from typical traumatic fractures. These fractures commonly arise from conditions that compromise integrity, such as metastatic cancer spreading to the (most frequently from primary sites like the , , , , or ), primary tumors (benign or malignant), , , Paget's disease, or infections like . metastases are a leading cause, affecting approximately 5% of the 2,041,910 projected annual cancer patients in the United States as of 2025, with about 8% of those with involvement experiencing a pathologic fracture. The most affected sites include the spine, proximal , , , and ribs, where osteolytic lesions from tumor-induced activation erode structure, leading to biomechanical failure even under normal loads. Symptoms typically include sudden or gradual at the fracture site, often worsening with movement or , along with swelling, tenderness, bruising, , and limited mobility; in some cases, the may occur spontaneously without noticeable trauma. involves a combination of clinical evaluation, imaging such as X-rays (which reveal lytic or blastic lesions), MRI or CT scans for detailed assessment, bone for detecting metastases, and laboratory tests like or metabolic panels to identify underlying causes, with confirming in suspicious cases. Management focuses on stabilizing the , treating the underlying condition, and preventing complications; non-surgical options include immobilization with casts or splints and control, while surgical interventions such as (plates, intramedullary nails), prosthetic replacement, or prophylactic stabilization for impending fractures (guided by criteria like Mirels' score) are often necessary, particularly in metastatic cases where radiotherapy or addresses the primary disease. Prognosis varies widely based on the etiology—for instance, patients with metastases have a 98% six-month survival rate, compared to 50% for —but healing generally takes several months, with risks of , , or further fractures if the underlying weakness persists. Prevention emphasizes early detection and management of predisposing conditions, such as bisphosphonates or for and bone metastases, alongside lifestyle measures like calcium/ intake and .

Overview

Definition and Classification

A pathologic fracture is defined as a bone break that occurs through abnormal or weakened due to an underlying process, such as a or , leading to failure under minimal trauma or even spontaneously—conditions that would not fracture healthy . This contrasts with traumatic fractures, which result from high-energy forces applied to structurally normal , emphasizing biomechanical compromise rather than the magnitude of applied stress. Pathologic fractures are classified primarily by the underlying into neoplastic and non-neoplastic categories. Neoplastic causes involve primary tumors, which may be benign (e.g., ) or malignant (e.g., ), or secondary metastatic lesions from distant primaries such as , , or cancers, which erode integrity through tumor invasion and osteolysis. Non-neoplastic causes stem from systemic or local conditions that impair quality without tumor involvement, including metabolic disorders like (characterized by reduced bone density) and (due to defective mineralization). Other examples include Paget disease of , which causes abnormal remodeling and cortical thinning. Further subclassification considers fracture characteristics and location. By pattern, fractures are complete (extending fully across the ), incomplete (partial disruption, often seen in trabecular ), or impending (a high-risk state without actual breakage, defined by significant structural compromise such as greater than 50% cortical destruction in weight-bearing bones). Impending fractures are assessed using tools like the Mirels score, which evaluates four components— site (: 1 point, lower limb: 2, peritrochanteric: 3), pain (mild: 1, moderate: 2, functional: 3), size (<1/3 diaphyseal width: 1, 1/3–2/3: 2, >2/3: 3), and radiographic appearance (blastic: 1, mixed: 2, lytic: 3)—with a total score exceeding 8 indicating prophylactic intervention to prevent actual . Common locations include long bones (e.g., , ), spine (vertebral compression), and , where weakened areas are prone to collapse under normal loads.

Epidemiology

Pathologic fractures represent a significant clinical burden, particularly in the context of underlying malignancies. , an estimated 2,041,910 new cancer cases are diagnosed annually, with approximately 5% of these patients developing metastases that predispose them to fractures, of whom approximately 8% experience a fracture. The overall incidence of pathologic fractures is increasing, driven by advances in cancer and treatment that extend survival times, allowing more patients to reach stages where skeletal complications manifest. Globally, the prevalence of fractures is estimated at about 28% among patients with metastatic , though this varies by and underlying condition. These fractures are most frequent in specific cancers: up to 43% of patients with experience them at diagnosis, followed by 35% in , 17-25% in , and around 19% in . Primary bone and sarcomas, though rarer, contribute to cases, with approximately 13,000 new sarcomas and 3,600 bone sarcomas diagnosed annually in the . Demographically, pathologic fractures are far more common in adults over 40 years of age, where the likelihood of a causing fracture being metastatic is 500 times greater than it being a primary . Gender patterns show a skew toward females in cases related to —a non-neoplastic cause weakening —while males predominate in prostate cancer-associated fractures. Geographically and temporally, rates are rising in developed countries due to aging populations and enhanced oncology care prolonging life expectancy in cancer patients. This trend underscores the growing need for preventive strategies in high-risk groups.

Etiology

Neoplastic Causes

Neoplastic causes of pathologic fractures primarily arise from tumors that compromise bone integrity through direct invasion, osteolysis, or excessive bone formation. Metastatic disease is the most common cause, accounting for the majority of such fractures, originating from various primary malignancies that spread hematogenously to bone, leading to involvement in 30-75% of advanced cases depending on the cancer type. Common primaries include breast cancer, which produces predominantly osteolytic lesions but can also cause mixed or osteoblastic changes; lung cancer, typically resulting in purely lytic destruction; prostate cancer, characterized by osteoblastic reactions; and renal cell carcinoma or thyroid cancer, both often lytic in nature. These metastases weaken cortical bone, increasing fracture risk, with breast cancer being a leading cause. Primary bone tumors, in contrast, are rare, comprising only 1-2% of neoplastic pathologic fractures, as they represent less than 1% of all malignancies overall. These tumors elevate fracture risk through rapid proliferation and cortical erosion. , the most common primary malignant , predominantly affects adolescents and arises in the of long bones, such as the distal or proximal . occurs mainly in children and involves the of long bones, like the or . , more typical in adults over 40, frequently develops in the or proximal /, leading to insidious bone weakening and fracture. Tumors in both metastatic and primary contexts induce via activation of osteoclasts, primarily through the RANKL (receptor activator of nuclear factor kappa-B ligand) pathway, where tumor cells or stromal interactions upregulate expression, promoting focal osteolysis and structural compromise. This mechanism underlies the diffuse lytic lesions seen in , a hematologic that causes pathologic fractures in up to 43% of patients. Impending fracture risk in these cases is evaluated using the Mirels scoring system, which sums points across four criteria: site ( = 1, lower limb = 2, peritrochanteric = 3), pain (mild = 1, moderate = 2, functional = 3), lesion type (blastic = 1, mixed = 2, lytic = 3), and size (less than 1/3 of bone diameter = 1, 1/3 to 2/3 = 2, greater than 2/3 = 3); a total score exceeding 7 indicates high risk and consideration for prophylactic intervention.

Non-Neoplastic Causes

Non-neoplastic causes of pathologic fractures encompass a range of systemic and local conditions that weaken integrity without involving , including metabolic bone diseases, infections, and other disorders such as or endocrine abnormalities. Metabolic bone diseases represent a primary category, with being the most prevalent etiology, particularly in postmenopausal women and the elderly due to reduced density from imbalanced remodeling. This condition predisposes individuals to fractures in weight-bearing sites like the vertebrae, , and , often occurring with minimal trauma. is a leading cause of pathologic fractures in older adults. Osteomalacia, resulting from vitamin D deficiency or impaired mineralization, leads to softened bones and increased fragility, manifesting as looser zone fractures or complete breaks in long bones and ribs. This disorder is less common than but significantly elevates through defective bone matrix formation. Paget's disease of bone involves disordered remodeling with excessive activity followed by chaotic response, resulting in enlarged, deformed, and brittle bones, commonly affecting the , , and long bones. This leads to a heightened , estimated at up to several-fold higher than in unaffected individuals, due to structural weakening. Infectious causes primarily include , a bacterial often due to , which erodes cortical bone through inflammation and formation, culminating in fractures of s as a rare but serious complication. Chronic increases this risk by persistent bone destruction, with fractures reported in 1-2% of cases involving long bone shafts. Tuberculous spondylitis, known as , causes chronic vertebral destruction via granulomatous infection, leading to compression fractures and kyphotic deformities from bone and collapse. This form often presents insidiously with mimicking degenerative changes. Other non-neoplastic etiologies include radiation-induced bone changes, where prior radiotherapy for adjacent malignancies causes osteonecrosis and vascular compromise, fracturing irradiated fields with an incidence ranging from 1% to 25%, particularly in the , , and extremities. promotes excessive , forming brown tumors—benign osteolytic lesions that weaken bone and precipitate fractures, often in the , long bones, or spine. Fibrous dysplasia, a benign fibro-osseous disorder typically in children and young adults, replaces normal bone with fibrous tissue, rendering sites like the or prone to pathologic fractures due to cortical thinning.

Pathophysiology

Mechanisms of Bone Weakening

Pathologic fractures arise from underlying diseases that compromise bone integrity through various cellular and mechanical pathways, primarily involving dysregulated bone remodeling. In osteolytic processes, prevalent in conditions such as skeletal metastases and multiple myeloma, tumor cells stimulate osteoclast hyperactivity by secreting factors like parathyroid hormone-related protein (PTHrP) and receptor activator of nuclear factor kappa-B ligand (RANKL). PTHrP, commonly produced by breast and lung cancer metastases, mimics parathyroid hormone to enhance osteoclast differentiation and activity via cyclic AMP-mediated pathways, leading to excessive bone resorption. Similarly, in multiple myeloma, malignant plasma cells upregulate RANKL expression on osteoblasts and stromal cells, binding to RANK on osteoclast precursors to promote their maturation and survival, resulting in focal cortical thinning and the formation of lytic lesions that act as stress risers. This resorption can reduce bone volume by up to 30%, causing up to 30% loss in mechanical strength, as the remaining trabecular architecture becomes insufficient to withstand normal physiological loads. Angiogenesis further exacerbates osteolytic weakening by facilitating lesion expansion; tumor-derived (VEGF) and interleukin-8 (IL-8) promote neovascularization, which supplies nutrients to proliferating tumor cells and osteoclasts, accelerating bone destruction at the lesion periphery. These localized defects disrupt the bone's uniform load distribution, creating stress concentrations where normal forces exceed the material's yield strength, predisposing to under minimal trauma. In contrast, osteoblastic responses, observed in metastases from or cancers, involve excessive woven bone formation driven by tumor-secreted endothelin-1 (ET-1) and bone morphogenetic proteins (BMPs). ET-1 activates proliferation and mineralization through endothelin receptors, while BMPs, particularly and BMP-4, induce differentiation of mesenchymal stem cells into s, leading to disorganized, immature bone deposition. This hyperostotic bone lacks the organized of normal cortical bone, rendering it brittle and susceptible to fatigue failure from repetitive loading, despite apparent increased density on imaging. Biomechanically, both lytic and blastic alterations compromise bone's ability to resist deformation. Lytic lesions function as notches, amplifying local stresses according to principles, where progressive microdamage accumulates without adequate repair, culminating in impending or complete . Specific predictors include greater than 50% cortical destruction in long bones, which significantly elevate fracture risk by reducing the bone's and load-bearing capacity. These thresholds highlight how localized weakening transforms routine activities into high-risk events for structural failure.

Clinical Features

Symptoms

Patients with pathologic fractures often experience prodromal symptoms weeks to months prior to the event, primarily manifesting as localized, persistent that worsens at night or with activities due to periosteal from underlying lesions. This pain commonly serves as a key warning sign of impending . Upon acute , patients typically report sudden, severe pain at the site, accompanied by localized swelling, deformity, and inability to bear weight, particularly in long bones like the or . For spinal pathologic fractures, which account for a substantial portion of cases, acute symptoms include intense as the most common presentation, often with associated such as numbness, tingling, or weakness in the extremities due to involvement; in severe instances, may lead to bowel or bladder dysfunction. In non-neoplastic causes such as or , symptoms may be more insidious, with gradual onset of pain during routine activities rather than a distinct , though acute pain remains similar to neoplastic cases. Associated systemic symptoms arise from the underlying disease process and may include , fatigue, and anorexia in patients with malignancies such as or metastatic cancer. In cases involving lytic bone metastases, hypercalcemia can contribute additional symptoms like , , , and . For hematologic malignancies like or myeloma, such as fever, night sweats, and further may accompany the localized complaints.

Physical Examination Findings

During physical examination of a suspected pathologic fracture, local signs at the affected site commonly include tenderness upon , localized swelling, ecchymosis, and in displaced cases. Limited due to pain and guarding is frequently observed, along with instability elicited by , such as in fractures. Deformity may manifest as apparent shortening or abnormal rotation of the affected limb in fractures, often leading to disturbances or antalgic . Functional assessment reveals potential neurovascular deficits, including weakness or from peroneal nerve involvement in lower extremity fractures. Systemic signs in malignancy-associated pathologic fractures can include evidenced by unintentional weight loss and muscle wasting, as well as palpable . Signs of hypercalcemia, such as or altered mental status with , may also be present. In spinal pathologic fractures, localized tenderness over the vertebrae is noted, accompanied by neurological deficits like or sensory changes suggestive of cord compression. Specific to femoral pathologic fractures from metastatic disease, patients often present with inability to walk or bear weight, highlighting the functional impact. Neurovascular compromise, though uncommon overall, occurs in some cases—particularly with spinal or vascular proximity—and necessitates urgent evaluation to prevent irreversible damage.

Diagnosis

Imaging Techniques

Plain radiography serves as the initial imaging modality for suspected pathologic fractures, providing essential visualization of bone integrity and underlying lesions. It typically reveals fracture lines traversing areas of weakened bone, such as lytic or blastic lesions, cortical destruction, and aggressive features including periosteal reaction or lesions exceeding 5 cm in size. In metastatic disease, plain radiographs often demonstrate osteolytic patterns, which are common in metastases from primaries like breast or lung cancer (approximately 70-80% lytic in breast cancer), but vary by primary site (e.g., more blastic in prostate cancer); they may appear as punched-out or moth-eaten erosions particularly in multiple myeloma. Orthogonal views of the fracture site and the entire affected bone are recommended, along with a chest radiograph to screen for primary malignancies. Advanced imaging techniques offer enhanced characterization of pathologic fractures, assessing extent, involvement, and multifocal disease. (MRI) excels in evaluating marrow infiltration and extension, showing T1-hypointense lesions with corresponding T2 hyperintensity or STIR enhancement; it achieves sensitivities of 91-100% for detecting metastases and is urgently indicated for suspected via targeted spinal protocols. Computed tomography (CT) provides detailed fracture patterns and cortical involvement, identifying impending fractures when more than 50% of the cortex is destroyed; it is particularly useful for preoperative planning and guidance, with sensitivities ranging from 71-100%. using detects multifocal osteoblastic activity as hot spots in up to 90% of metastatic cases, serving as a standard whole-body protocol for staging. Positron emission tomography-computed tomography (PET-CT) integrates metabolic activity assessment, highlighting hypermetabolic tumors with high sensitivity for , though specificity is typically greater than 95% when combined with CT ; it is valuable for detecting lesions and monitoring response in neoplastic causes. Emerging modalities like 18F-sodium (18F-NaF) PET/CT offer improved sensitivity (>90%) for bone metastases detection. For , skeletal surveys via plain radiography or low-dose whole-body CT are preferred over due to the purely lytic nature of lesions, which may not uptake tracer. These modalities collectively guide differentiation from non-pathologic fractures by revealing endosteal scalloping, masses, or permeative destruction absent in stress injuries.

Laboratory Evaluation and Biopsy

Laboratory evaluation for pathologic fractures begins with a (CBC), which may reveal in cases associated with due to bone marrow infiltration by plasma cells. can indicate an underlying contributing to bone weakening and fracture. A is essential, focusing on serum calcium levels, as hypercalcemia often occurs in lytic bone diseases such as or metastases, resulting from osteoclast activation and calcium release from resorbed bone. (ALP) levels are commonly seen in conditions like Paget's disease or , reflecting increased bone turnover. Tumor markers are selected based on suspected primary malignancies; for instance, prostate-specific antigen (PSA) is useful in evaluating metastases, while cancer antigen 15-3 (CA 15-3) aids in monitoring with bone involvement, where elevated levels correlate with metastatic spread. In suspected , (SPEP) is performed to detect a monoclonal protein (M-spike), present in approximately 80% of cases, confirming the diagnosis when combined with other findings. Biopsy is indicated following to confirm the underlying , particularly in cases of unknown primary tumors, which account for about 10-25% of metastatic presentations. Techniques include imaging-guided core needle or open , with the former preferred for its minimally invasive nature and high diagnostic yield. Histopathological analysis distinguishes tumor types, such as from in neoplastic cases, or identifies metabolic changes like thin trabeculae in for non-neoplastic causes. confirms the in up to 97% of cases when adequately performed, often integrated after initial TNM staging to guide management of metastases. Risks include tumor seeding along the tract, which is rare (less than 2% with modern techniques), though this rate is minimized with proper technique.

Management

Conservative Approaches

Conservative management of pathologic fractures is primarily indicated for stable, non-displaced fractures in patients with low risk of progression or limited life expectancy, focusing on pain relief, fracture stabilization, and addressing the underlying etiology without surgical intervention. Immobilization techniques, such as bracing or casting, are employed for stable pathologic fractures to promote healing and prevent further displacement, particularly in weight-bearing bones or the spine. For instance, vertebral body braces are commonly used for spinal pathologic fractures to maintain alignment and reduce pain. These approaches are recommended for lesions with a low Mirels score (less than 7), where the risk of fracture progression is minimal, or in patients with a short life expectancy of less than 3 months, for whom invasive procedures may not be beneficial. Pharmacotherapy plays a central role in symptom control and reducing skeletal complications. Analgesics, including opioids for severe , are essential for managing acute discomfort associated with the fracture. Bisphosphonates and inhibit activity, thereby reducing skeletal-related events such as pathologic fractures by 31-41% in patients with bone metastases from cancers like , , or . serves as a palliative option for painful lesions, typically delivered as 30 Gy in 10 fractions, providing complete in 31% of cases for radiosensitive tumors such as myeloma, , , or cancers, and partial in 54%. This modality can also help prevent progression to fracture in impending cases by promoting remineralization. Treatment of the underlying disease is integral to conservative strategies. For neoplastic causes, or hormonal therapies, such as for metastases, target the primary malignancy to halt bone destruction. In infectious etiologies, antibiotics are administered to control the underlying , often in combination with immobilization to support fracture healing. Such conservative measures are suitable for patients with expected survival under 3 months, prioritizing over aggressive intervention.

Surgical Interventions

Surgical interventions for fractures are indicated in cases of unstable fractures, such as those with displacement or greater than 50% destruction, impending fractures assessed by a high Mirels score greater than 8, or when neurovascular compromise is present; the primary goals are to restore function, enable early mobilization, and alleviate . Prophylactic surgery is particularly recommended for lesions in bones to prevent complete and associated morbidity, especially in patients with expected survival exceeding 3-6 months. Common techniques include intramedullary nailing for diaphyseal fractures of long bones like the and , which provides internal stabilization with minimal soft-tissue disruption and facilitates early . For periarticular fractures, plate and screw fixation offers precise alignment and allows for tumor , while endoprosthetic replacement is preferred for extensive proximal lesions in the or to achieve immediate stability. In spinal pathologic fractures, vertebroplasty involves injection of into the vertebral body, and kyphoplasty uses balloon tamping prior to cement augmentation to restore height and reduce ; these minimally invasive procedures are suitable for osteolytic compression fractures without instability. Adjuvant measures often incorporate polymethylmethacrylate (PMMA) cement to fill lytic defects and augment fixation, enhancing mechanical stability particularly in osteoporotic or metastatic bone. For solitary metastases in patients with prolonged expected survival, wide resection followed by reconstruction may be performed to address the underlying tumor burden. These interventions generally allow early ambulation and improve mobility in the majority of patients, with vertebroplasty and kyphoplasty providing marked pain relief in approximately 84% of cases involving metastatic . Complication rates range from 10% to 30%, with common issues including (8-12%) and hardware failure (up to 17%), particularly in lower limb lesions where surgical stabilization is prioritized to support weight-bearing.

Prognosis and Complications

Survival Outcomes

Pathologic fractures signify advanced underlying , often indicating widespread metastatic disease and thereby substantially reducing overall patient survival. The 6-month survival rates following such fractures vary significantly by primary tumor type, with patients exhibiting the highest rate at 98%, followed by at 89%, at 51%, and at 50%. Several factors influence survival outcomes in patients with pathologic fractures. The primary tumor type is a key determinant, with hormone-sensitive cancers such as and generally conferring better due to responsiveness to systemic therapies, whereas aggressive primaries like and are associated with poorer outcomes. Fracture location plays a role as well, with spinal fractures linked to worse survival owing to heightened risks of neurological complications, spinal instability, and cord compression. Additionally, patient profoundly affects ; an Eastern Cooperative Oncology Group (ECOG) score greater than 2 is associated with roughly halved survival compared to lower scores, reflecting diminished functional reserve and treatment tolerance. Specific data underscore these trends in certain malignancies. In , the occurrence of pathologic fractures correlates with increased mortality risk compared to patients without fractures, attributable to exacerbated skeletal morbidity and progression. Overall, pathologic fractures from bone metastases elevate mortality risk relative to metastatic without fracture, highlighting their role as a marker of frailty and accelerated decline. Complications arising from pathologic fractures further compromise survival. Hypercalcemia, driven by osteolytic activity in metastatic lesions, can be fatal if untreated due to cardiac arrhythmias, renal failure, and altered mental status. Postoperative infections following surgical stabilization contribute to and prolonged hospitalization that worsen outcomes. , exacerbated by immobility and hypercoagulability in cancer, is a frequent that heightens the risk of and multiorgan failure.

Preventive Measures

Preventive measures for fractures focus on identifying at-risk individuals early and implementing interventions to strengthen integrity or stabilize lesions before breakage occurs. In patients with high-risk malignancies such as , routine screening with (DXA) scans is recommended at baseline and periodically to assess bone mineral density (BMD), as myeloma-induced bone loss increases fracture susceptibility. Emerging AI-based predictive models are also being developed to refine fracture risk assessment beyond traditional tools like the Mirels score. For metastatic disease, the Mirels scoring system evaluates impending risk based on site, pain, lesion size, and radiographic appearance; scores of 8 or higher typically warrant consideration for prophylactic surgical intervention to avert . Pharmacologic strategies play a central role in reducing skeletal-related events (SREs), including fractures, particularly in patients with bone metastases from cancers like or . Intravenous bisphosphonates, such as , inhibit activity and have been shown to decrease the incidence of SREs by approximately 25-30% when initiated early in the course of metastatic disease. , a targeting , demonstrates superior efficacy to in preventing fractures in some randomized trials, with a of up to 18% for SREs in patients with bone metastases. Supplementation with calcium and is advised for patients with underlying to support BMD and modestly lower fracture risk, especially in those receiving cancer therapies that exacerbate bone loss. Lifestyle modifications and supportive therapies further mitigate risk by enhancing bone health and minimizing mechanical stress on weakened sites. Weight-bearing exercises, such as walking or resistance training, promote and improve balance, thereby reducing fall-related fracture incidence in at-risk elderly patients. programs, including home safety assessments and balance training, are particularly beneficial for older adults with metastatic disease. Adjuvant treatments like or systemic can stabilize bone lesions by reducing tumor burden, preventing progression to fracture when applied to impending lesions. Prophylactic surgical fixation, such as intramedullary nailing of the in high-risk metastatic lesions (Mirels score ≥8), prevents actual in the majority of cases and helps maintain ambulation while avoiding complications. Early integration of these measures in multidisciplinary care for underlying diseases can substantially lower the overall burden of pathologic fractures.

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