This article presents a unified clinical theory
that links established facts about the physiology of bone and homeostasis,
with those involved in the healing of fractures and the development
of nonunion. The key to this theory is the concept that the tissue
that forms in and around a fracture should be considered a specific
functional entity. This ‘bone-healing unit’ produces a physiological
response to its biological and mechanical environment, which leads
to the normal healing of bone. This tissue responds to mechanical
forces and functions according to Wolff’s law, Perren’s strain theory
and Frost’s concept of the “mechanostat”. In response to the local
mechanical environment, the bone-healing unit normally changes with
time, producing different tissues that can tolerate various levels
of strain. The normal result is the formation of bone that bridges
the fracture – healing by callus. Nonunion occurs when the bone-healing
unit fails either due to mechanical or biological problems or a
combination of both. In clinical practice, the majority of nonunions
are due to mechanical problems with instability, resulting in too
much strain at the fracture site. In most nonunions, there is an
intact bone-healing unit. We suggest that this maintains its biological
potential to heal, but fails to function due to the mechanical conditions.
The theory predicts the healing pattern of multifragmentary fractures
and the observed morphological characteristics of different nonunions.
It suggests that the majority of nonunions will heal if the correct
mechanical environment is produced by surgery, without the need
for biological adjuncts such as autologous bone graft. Cite this article:
We determined the efficacy of a devitalised autograft
(n = 13) and allograft (n = 16) cortical strut bone graft combined
with long-stem endoprosthetic reconstruction in the treatment of
massive tumours of the lower limb. A total of 29 patients (18 men:11
women, mean age 20.1 years (12 to 45) with a ratio of length of
resection to that of the whole prosthesis of >
50% were treated
between May 2003 and May 2012. The mean follow-up was 47 months
(15 to 132). The stem of the prosthesis was introduced through bone
graft struts filled with cement, then cemented into the residual
bone. Bone healing was achieved in 23 patients (86%). The mean Musculoskeletal
Tumour Society functional score was 85% (57 to 97). The five-year
survival rate of the endoprostheses was 81% (95% confidence intervals
67.3 to 92.3). The mean length of devitalised autografts and allografts
was 8.6 cm (5 to 15), which increased the ratio of the the length
of the stem of the prosthesis to that of the whole length of the
prosthesis from a theoretical 35% to an actual 55%. Cortical strut bone grafting and long-stem endoprosthetic reconstruction
is an option for treating massive segmental defects following resection
of a tumour in the lower limb. Patients can regain good function
with a low incidence of aseptic loosening. The strut graft and the
residual bone together serve as a satisfactory bony environment
for a revision prosthesis, if required, once union is achieved. Cite this article:
This review is aimed at clinicians appraising
preclinical trauma studies and researchers investigating compromised bone
healing or novel treatments for fractures. It categorises the clinical
scenarios of poor healing of fractures and attempts to match them
with the appropriate animal models in the literature. We performed an extensive literature search of animal models
of long bone fracture repair/nonunion and grouped the resulting
studies according to the clinical scenario they were attempting
to reflect; we then scrutinised them for their reliability and accuracy
in reproducing that clinical scenario. Models for normal fracture repair (primary and secondary), delayed
union, nonunion (atrophic and hypertrophic), segmental defects and
fractures at risk of impaired healing were identified. Their accuracy
in reflecting the clinical scenario ranged greatly and the reliability
of reproducing the scenario ranged from 100% to 40%. It is vital to know the limitations and success of each model
when considering its application.
A number of causes have been advanced to explain the destructive discovertebral (Andersson) lesions that occur in ankylosing spondylitis, and various treatments have been proposed, depending on the presumed cause. The purpose of this study was to identify the causes of these lesions by defining their clinical and radiological characteristics. We retrospectively reviewed 622 patients with ankylosing spondylitis. In all, 33 patients (5.3%) had these lesions, affecting 100 spinal segments. Inflammatory lesions were found in 91 segments of 24 patients (3.9%) and traumatic lesions in nine segments of nine patients (1.4%). The inflammatory lesions were associated with recent-onset disease; a low modified Stoke ankylosing spondylitis spine score (mSASSS) due to incomplete bony ankylosis between vertebral bodies; multiple lesions; inflammatory changes on MRI; reversal of the inflammatory changes and central bony ankylosis at follow-up; and a good response to anti-inflammatory drugs. Traumatic lesions were associated with prolonged disease duration; a high mSASSS due to complete bony ankylosis between vertebral bodies; a previous history of trauma; single lesions; nonunion of fractures of the posterior column; acute kyphoscoliotic deformity with the lesion at the apex; instability, and the need for operative treatment due to that instability. It is essential to distinguish between inflammatory and traumatic Andersson lesions, as the former respond to medical treatment whereas the latter require surgery.
Between October 2001 and September 2009 we lengthened 242 lower-limb segments in 180 patients using the Intramedullary Skeletal Kinetic Distractor (ISKD). Mechanical failure was defined either as breakage of the ISKD or failure of the internal mechanism to activate. Retrieved nails which failed mechanically were examined by the manufacturer for defects. In all, 15 ISKDs in 12 patients (13 limbs) failed mechanically representing an overall failure rate of 6.2%, with fracture of the device occurring in ten of the 15 failures. Two nails in one patient failed to lengthen and had to be replaced. The manufacturer detected an error in the assembly of the nail, which prompted a wide recall. One nail jammed after being forcefully inserted, and two nails failed to lengthen fully. Lengthening was achieved in all 12 patients, although three required a second operation to exchange a defective nail for a new, functioning device. The ISKD is a complex mechanical device which lengthens by the oscillation of two telescopic sections connected by a threaded rod. The junction between these sections is surrounded by a keyring collar. This keyring collar is the weakest part of the device.
