The Journal of Bone and Joint Surgery (American) 83:971-986 (2001)
© 2001 The Journal of Bone and Joint Surgery, Inc.
Retrieved Human Allografts
A Clinicopathological Study
William F. Enneking, MD and
Domenico A. Campanacci, MD
Investigation performed at the Department of Orthopaedics
and Rehabilitation, University of Florida College of Medicine, Gainesville,
Florida
William F. Enneking, MD
Department of Orthopaedics and Rehabilitation, University of
Florida College of Medicine, Box 100246 JHM Health Center, Gainesville,
FL 32610-0246
Domenico A. Campanacci, MD
First University Clinic, Instituto Ortopedico Rizzoli, Via Pupilli
1, 40100 Bologna, Italy
No benefits in any form have been received or will be received
from a commercial party related directly or indirectly to the subject
of this article. No funds were received in support of this study.
Background: We studied seventy-three massive
preserved human allografts, retrieved from two to 156 months after
implantation, to provide insight into the mechanisms of their repair.
Methods: The specimens were studied with radiographic
and histological techniques that permitted time-related quantitative
analysis of the reparative mechanisms of union, cortical repair,
soft-tissue attachment, fracture, and characteristics of the allograft-cement interface
and the articular cartilage.
Results: Union at cortical-cortical junctions occurred slowly
(approximately twelve months) by host-derived external callus that
bridged the junction and filled the gap between abutting cortices.
The bone in the gap did not undergo stress-oriented remodeling even
after many years, and, when the union was intentionally disrupted,
failure occurred at the cement line that marked the allograft-host
junction. Repair of the necrotic graft matrix was both external
and internal. External repair consisted of the apposition of a thin
seam of host bone on the outer surface of the graft, coating about
40% of the surface at one year and 80% at two
years. Internal repair was confined to the ends and the periphery
of the cortices and penetrated so slowly that only 15% to
20% of the graft was repaired by five years, after which
deeper repair seldom occurred. Graft fractures in specimens retrieved
soon after fracture showed only necrotic bone adjacent to the fracture site,
whereas those retrieved after fracture-healing showed a marked increase
in internal repair of the bone about the fracture site. When bone
cement had been used to fix a prosthesis, there was no evidence of
bone resorption or loosening of the device.
The osteoarticular specimens showed no survival of chondrocytes
in the articular cartilage. However, the architecture of the acellular
cartilage was well preserved after two to three years and occasionally after
as many as five years. Late degenerative changes in the articular
cartilage coincided with subchondral revascularization and fragmentation, and
the articulating surfaces became covered by a pannus of fibrovascular
reparative tissue. Degenerative changes in articular cartilage occurred
earlier and were more advanced in specimens retrieved from patients
with an unstable joint than in those retrieved from patients with
a stable joint.
Conclusions: Repair of massive human allografts
is an indolent process that follows a fairly predictable course
during the first few years and is influenced by other biological
activities, such as fracture repair, supplementary autografting,
and tumor recurrence.
Clinical Relevance: These observations provide a
clear, detailed picture of the extent, timing, and deficiencies
in the incorporation and repair of large human allografts preserved
by conventional banking techniques. As such, they provide a basis
for comparative studies of the efficacy of the recently developed
osteoinductive substances currently under investigation.
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