440 Canine Sports Medicine and Rehabilitation
determined that the MoR is similar across
various breed conformations. They also con
firmed, by taking the BMD into account, that
most fractures occur between T9 and L7, as has
been determined clinically by retrospective
studies. The vertebral column’s chief structural
function is to resist dorsal and lateral bending.
Ventral bending is resisted predominately by
the abdominal musculature. This knowledge
should direct appropriate physical training
based on the anticipated functional results. Soft
tissue elements are critical support structures.
Muscular development and ligamentous
strength can decrease the forces placed upon
the spine. This may limit bony vertebral
strength and development, yet still be protec
tive. The exact combination of bony develop
ment and soft tissue development is unknown
and would be specific for the movements being
attempted. Obviously, special attention needs
to be given to core strength specifically to pro
tect the T9–L7 region (Zotti et al., 2011).
Repetitive motion conditions
In the canine athlete, practice and competition
has been directed to learning a complicated and
often forceful set of movements that can cause
damage as the work‐to‐failure ability of the soft
tissues or bones cannot absorb the repeated
stresses that occur without significant healing,
remodeling, and recovery. Dogs that do not
have obvious spinal cord issues have been char
acterized as having sore backs or sore necks.
With the wide availability of CT, degenerative
bony conditions can be described in detail, yet
these changes often are not correlated to
performance.
Soft tissue damage to the paraspinal struc
tures and joints in many cases may be the
source of spinal pain or poor performance.
These changes often can be appreciated with
MRI but few studies have evaluated this poten
tial source of spinal pain.
Repetitive stress to bones creates failures in
the bone matrix known as microfractures
(Frost, 1960; Lee et al., 2003). These microfrac
tures accumulate and are known to decrease
the stiffness of the bone and its ability to
absorb additional stress (Burr et al., 1998).
Healing of microfractures starts with resorp
tion of the surrounding bone matrix and may
decrease the ability of the bone to handle addi
tional stress until healing is complete (Carter
& Hayes, 1977). Microfractures are cumulative
and their ability to repair is decreased with
age in people. The association of bone failure
and microfractures is not linear with the stress
placed upon the bone. The ability of the
bone to withstand compressive forces is also
dependent upon the bone volume fraction
(bone volume/total volume) of the structure
being tested. Microfractures only start to accu
mulate when there is a stiffness loss in the
bone of approximately 15% (Burr et al., 1997).
Dogs whose microfractures were prevented
from healing by pharmacological methods
(Flora et al., 1981) or endocrine manipulation
(Norrdin et al., 1990) developed pathological
fractures. Compressive strength was decreased
in the lumbar and thoracic vertebrae even
though the bone volume was normal.
Hasegawa and colleagues (1995) determined
that surgical damage to the intervertebral
discs in dogs also increased the accumulation
of microfractures within the vertebrae.
Several important considerations come out of
these studies. Developing strong bones neces
sary to handle the stresses placed upon them
should be part of the training procedures to
produce long‐lasting successful canine athletes.
Strong soft tissue components involving core
strength can protect forces placed on the bones
and joints. Attention to bone and soft tissue
strength should be directed to vertebrae T9–L7
specifically. Adequate time between rigorous
activities has to be a consideration. There is a
period of time when bones are particularly
prone to stress once the microfractures have
occurred and the remodeling process further
decreases bone strength, as bone resorption is
the initial step in healing. Whether these
changes in bone strength and remodeling forces
are responsible for so‐called sore backs or are in
fact responsible for any of the osteoarthritic
changes noted in spinal studies, is an area that
requires further investigation. In addition, there
are numerous circumstances where interverte
bral disc degeneration is diagnosed with con
ventional radiography or advanced imaging. In
those cases, even when there are no overt neu
rological deficits, the biomechanics of the spine
are compromised (Burr et al., 1997).