Abstract
Background Spinal allografts are commonly used in vertebral reconstruction to provide structural support and facilitate fusion, particularly in cases involving extensive bone loss. Although graft nonunion and failure are recognized complications, these events are typically identified within the early or mid-term postoperative period. The long-term results of spinal allografts over decades remain poorly documented.
Case Presentation A 45-year-old woman with a 25-year history of disseminated hydatid disease who underwent lumbar hemivertebrectomy, cyst excision, posterior instrumentation, and bone allografting came to the emergency department with new symptoms. Despite prolonged cyclic albendazole therapy, she developed repeated lumbosacral and gluteal recurrences complicated by chronic secondary infections. Over time, progressive vertebral destruction, persistent drainage, and irreversible neurological deficits were seen, leaving the patient bedbound. Cultures during recurrent infections grew Streptococcus mitis/oralis and Finegoldia magna. More than 2 decades after the initial surgery, the patient presented to the emergency department with an open lumbar wound and extrusion of bone-like material, which was found to be the spinal allograft. The patient was managed with local wound care, antimicrobial therapy, and supportive treatment.
Conclusion This case shows that a spinal allograft can remain completely nonincorporated for decades in a severely compromised vertebral environment. Chronic cystic echinococcosis with secondary infection prevented graft revascularization, leaving the allograft biologically inert and resulting in very late extrusion. This unprecedented outcome underscores that long-term allograft behavior depends primarily on sustained biological conditions rather than surgical technique or initial stability.
Introduction
Bone grafting is a fundamental component of spinal surgery, particularly in vertebral reconstruction procedures requiring structural support and fusion.1,2 Allografts are commonly used in these situations because they eliminate donor-site morbidity and provide readily available structural graft material.2,3 Unlike autografts, however, spinal allografts lack intrinsic osteogenic potential, and their incorporation depends entirely on host-related factors, including local vascularity, mechanical stability, and biological environment.3 Under favorable conditions, spinal allograft incorporation occurs through revascularization and creeping substitution, with radiographic fusion typically reported within the first 1 to 2 years after surgery.3 Nevertheless, factors such as inflammation, poor vascular supply, surgical interventions, and infection are well recognized to impair graft incorporation.1 While nonunion and graft failure are known complications of spinal allograft use, the long-term fate of grafts that remain nonincorporated has rarely been addressed in the literature.
An important but overlooked aspect of allograft biology is the transient mechanical weakening that occurs during incorporation. Like autografts, allografts undergo initial osteoclastic resorption before new bone formation through creeping substitution.4 During this resorptive phase, cortical grafts experience significant loss of mechanical strength, creating a period of structural vulnerability for complications such as graft fracture, migration, or extrusion, particularly when grafts are subjected to sustained mechanical loading or when incorporation is impaired by infection or poor vascularity.4,5 While cortical autografts that successfully incorporate eventually regain mechanical strength within 6 to 12 months, cortical allografts face additional challenges: unlike autografts, allografts trigger a host inflammatory response leading to the formation of a fibrous tissue layer that encapsulates the graft, impeding vascular ingrowth and delaying, or preventing, complete integration.5 Furthermore, even when cortical allografts appear radiographically incorporated, histological studies demonstrate that they frequently remain as admixtures of viable and necrotic bone, with substantial portions escaping remodeling entirely.5
Cystic echinococcosis (CE) is a rare cause of vertebral destruction, characterized by infiltrative growth within cancellous bone due to the absence of a protective pericyst. The parasite spreads along intratrabecular spaces, leading to progressive trabecular destruction, compression of intraosseous vessels, ischemic necrosis, and disruption of the vascular network essential for graft incorporation.6,7 Despite combined surgical and medical treatment, recurrence rates remain high, and relapses may occur years after initial therapy, reflecting the chronic and persistent nature of the disease.8 Secondary bacterial infection, although uncommon, can further impair local bone biology. In addition, repeated surgeries and chronic inflammation compromise neovascularization and osteoprogenitor cell migration, creating an unfavorable biological environment for spinal allograft integration.9
In this case study, we report a unique patient with chronic spinal hydatid disease complicated by secondary infection, in which a spinal allograft placed during vertebral surgery remained completely nonincorporated for 25 years and ultimately extruded. This case highlights the potential for very late allograft failure in severely compromised vertebral environments and underscores the importance of biological factors in long-term graft survival.
Case Presentation
A 45-year-old woman with a chronic disseminated hydatid disease was first diagnosed with lumbar-spinal CE in 2000, for which she underwent hemivertebrectomy, cyst excision, posterior instrumentation, and grafting. The superior portion of the left iliac wing was also removed, and spinal stabilization hardware was placed. Following surgery, the patient developed progressive lower-extremity motor deficits and became bedridden. Since 2000, she had been taking cyclic albendazole therapy (28 days on and 15 days off).
In 2016, she underwent thoracic surgery for pulmonary hydatid cysts. Over the subsequent years, she experienced recurrent lumbosacral and gluteal hydatid lesions with intermittent secondary infections, requiring repeated evaluations by consultants in orthopedics, radiology, and infectious diseases.
In February 2023, ultrasound-guided puncture, aspiration, injection, and reaspiration of a left gluteal cyst was performed, and a drainage catheter was placed. A follow-up culture in March grew Streptococcus mitis/Streptococcus oralis, for which she received intramuscular ceftriaxone. In July 2023, worsening pain and erythema over the gluteal region prompted repeat percutaneous drainage; 200 mL of purulent fluid was aspirated, yielding Finegoldia magna on anaerobic culture.
Later in July 2023, the patient presented to the emergency department with fever, tachycardia, and severe left leg pain. Laboratory work-up revealed anemia (Hb 6.1 g/dL), elevated inflammatory markers (C-reactive protein 40 mg/L and erythrocyte sedimentation rate 51 mm/h), and normal leukocyte and procalcitonin levels. Computed tomography imaging showed a destructive hydatid lesion involving L3 to L5 and the sacrum, with multiple daughter vesicles in the prevertebral space, right psoas, and right iliac fossa. Additional findings included numerous hydatid cysts throughout both lungs. Infectious diseases recommended albendazole (400 mg twice daily) and oral clindamycin for the anaerobic infection. Despite counseling regarding the risks, the patient left the hospital against medical advice.
In October 2025, she returned with a 15-day history of a new open wound over the lumbar midline. The patient’s main concerns were lumbar pain, purulent drainage from the lumbosacral region, and a bone-like material visible through the wound. During physical examination, a 3 × 2 cm full-thickness ulcer over the lumbar spine and 2 prior drainage sites over the sacral region were seen, and the bone allograft was visible through the ulcer, with no evidence of remodeling or fusion (Figure 1). Bilateral lower-extremity motor strength was 1/5. The patient was bedridden, fully dependent for activities of daily living, and required long-term caregiver support. On the computed tomography images, extensive destructive changes involving the L4 and L5 vertebrae, sacrum, and left iliac bone were seen, with bilateral gluteal abscess (Figure 2). Multiple cystic hydatid lesions, measuring up to 5 cm, were observed at the prevertebral space at L5, right iliac fossa, and the posterior to right psoas muscle. Pulmonary hydatid cysts were also visible in both lung fields. Magnetic resonance imaging from follow-up visits demonstrated progressive vertebral destruction and recurrent cystic lesions over time, reflecting ongoing disease activity and severe biological compromise (Figure 3). No further surgical intervention was planned. Ongoing management focused on wound care, infection control, and supportive treatment.
(a) Photograph of spinal allograft extruding through the lumbar wound, showing no evidence of biological remodeling. (b) Clinical photograph of the lumbar wound showing a full-thickness ulcer and drainage.
(a) Anteroposterior and lateral radiographs of the lumbosacral spine obtained during the patient’s emergency department visit, showing bone destruction, residual spinal instrumentation, and drainage catheters. (b) Computed tomography images (sagittal and coronal reconstructions) demonstrating near-complete destruction of the L4–L5 vertebral bodies, sacrum, and left iliac bone, with associated bilateral gluteal abscesses and multiple cystic lesions consistent with recurrent spinal hydatid disease.
Sagittal and axial magnetic resonance imaging of the lumbosacral spine obtained in 2007 (a), 2011 (b), 2018 (c), 2023 (d), and 12 October 2025 (e). Images demonstrate progressive vertebral destruction involving the lower lumbar vertebrae and sacrum with recurrent lesions, multiple daughter cysts, and extensive soft-tissue involvement. Serial imaging highlights ongoing disease progression, chronic infection, and failure of biological integration within a severely compromised vertebral environment.
Written informed consent was obtained from the patient for publication of this case report and accompanying images.
Discussion
Spinal CE is a rare but aggressive disease that frequently leads to progressive vertebral destruction and long-term morbidity. In this case, chronic disease, repeated recurrences, secondary infections, and severe neurological impairment created a profoundly unfavorable biological environment for bone healing. The most distinctive finding of this report is the behavior of the spinal allograft, which remained completely nonincorporated for 25 years and ultimately extruded.
Massive structural allografts are widely used for anterior column reconstruction following corpectomy in trauma, tumor, infection, and deformity surgery. Their primary indication is restoration of structural stability when large defects preclude autograft use. Despite providing immediate mechanical support, their incorporation is biologically demanding. Dense cortical architecture limits surface area for vascular ingrowth, and remodeling depends on gradual creeping substitution from the host bone-graft interface.10,11 Even under favorable conditions, incomplete remodeling, delayed union, graft fracture, subsidence, and pseudarthrosis have been reported, particularly in oncological or infected settings.11,12 Thus, structural stability does not necessarily equate to biological incorporation. This distinction is particularly critical in environments where host vascularity and immune competence are compromised.
Previous studies evaluating spinal allograft incorporation have largely focused on short- to mid-term outcomes. Graft nonunion or pseudarthrosis is typically identified within the first few postoperative years, and follow-up durations rarely exceed 5 to 10 years.13,14 Even in vertebral reconstruction for infection or tumor-related defects, graft failure is generally recognized early. No previous report has described a spinal allograft remaining biologically inert for more than 2 decades before late extrusion.
Chronic infection is a well-established factor impairing bone healing and graft incorporation. In osteomyelitis, devascularized bone may become sequestered and act as a persistent nidus for infection.15 While sequestrum formation is well described in native bone, its relevance to structural spinal allografts has rarely been emphasized. In this case, long-standing parasitic disease combined with recurrent secondary bacterial infection likely prevented revascularization and remodeling, resulting in permanent nonintegration of the graft.
Secondary bacterial infection in spinal hydatid disease, although rare, represents a severe complication associated with chronic drainage and limited reconstructive options.7 Under these conditions, reconstructive goals may shift from achieving fusion to disease control. This case demonstrates that in a persistently hostile biological environment, spinal allografts may remain permanently nonincorporated and eventually extrude, even decades after implantation.
This report expands the literature by showing that allograft nonincorporation may persist indefinitely in chronic parasitic disease. While early graft failure is recognized, late extrusion following prolonged biological inactivity has not previously been described. These findings suggest that long-term graft fate is governed primarily by biological viability rather than mechanical reconstruction alone.
The principal strength of this report is the exceptionally long follow-up period. Limitations include the single-patient design, absence of histopathological analysis of the extruded graft, and incomplete longitudinal clinical data.
Conclusion
This case shows that an allograft can remain completely nonincorporated for decades in a severely compromised environment. Chronic CE with secondary infection prevented graft revascularization, leaving the allograft inert and resulting in very late extrusion. This outcome highlights that long-term allograft behavior depends primarily on biological conditions rather than surgical technique or stability.
Footnotes
Funding The authors received no financial support for the research, authorship, and/or publication of this article.
Declaration of Conflicting Interests The authors report no conflicts of interest in this work.
- This manuscript is generously published free of charge by ISASS, the International Society for the Advancement of Spine Surgery. Copyright © 2026 ISASS. To see more or order reprints or permissions, see http://ijssurgery.com.
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