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Accordingly, two pathways that are in accordance with the criteria postulated by Bogduk (2005)
have been deemed as a cause to develop LBP (Fig. 1.8). LBP is based primarily (I) on the
mechanical disruption of the spine support structures (tendons, nerves, muscles, bones, ligaments,
discs), where the integrity of the tissues is violated and their mechanical order perturbed either by
exposure to high or to repeated and prolonged relative low stresses (load-tolerance mismatch), and
(II) on muscle function disruption, where trunk muscles functioning and “balance” between muscles’
intensities are disrupted by physiological, biochemical or mechanical mechanisms (Bogduk, 2005;
Kumar, 2001; Marras, 2008; McGill, 2007; Roy and DeLuca, 1996; Solomonow, 2004, 2009;
Zernicke and Whiting, 2000).
1.5.3.1.
Tissues’ Mechanical Disruption
Body movements are powered and controlled by the force produced by the contractions of the
skeletal muscles that is transmitted via its associated tendons to the skeleton to produce a musculotendinous moment of force at the joint axes modulated by the length and velocity of each motor
unit, and by the interaction of the musculotendinous moment of force with the external forces that
are transmitted to the body from the environment (Winter, 2009). The external forces, and the
forces that are generated internally by muscle contractions and by the passive reactions of tendons,
ligaments and fascia to muscle and/or external forces, also act on spine’s supporting structures,
either directly like in the musculotendinous union, or indirectly transmitted through other tissues
like the compression and shear stresses developed in the intervertebral disks during trunk bending
(McGill, 2007).
LBP related to the spine’s supporting structures can be developed in two different ways both arising
within the load-tolerance framework of Fig. 1.6 (Ayoub and Woldstad, 1999; Chaffin, Andersson,
and Martin, 2006; Kumar, 1999, 2001; Marras, 2008; McGill, 1997, 2007; NRC-IOM, 2001; Op de
Beek and Hermans, 2000; Pećina and Bojanić, 2004; Radwin, Marras, and Lavender, 2002). This
is because the tissue load can exceed the tissue tolerance in two ways: (I) the load can increase
or (II) the tolerance can decrease (Fig. 1.7). On one hand, it is the acute trauma injury, arising
from a single and identified event where the load exceeds the failure tolerance of the tissue or the
ability of the support structure to withstand the load, and on the other hand, it is the time-varying
cumulative disorder, which result from the accumulated effect of transient external loads that, in
isolation, are insufficient to exceed tissues tolerances, but when repeated or sustained loads are
applied for a prolonged time the internal tolerances of the tissues or the ability of the structure to
withstand the load are eventually exceeded (Radwin, Marras, and Lavender, 2002).
Cumulative disorders are caused by a repeated micro-trauma caused by continuous exposure to
mechanical strain that overwhelms the tissue’s ability to repair itself from the micro-damages
and therefore biological adaptation cannot take place (Kumar, 2001; Pećina and Bojanić, 2004).
This is because micro-damages depend on viscoelastic characteristics of biological tissues where
the repeated or sustained application of load to a tissue tends to wear it down, thus, lowering
its mechanical tolerance to the point where the tolerance is exceeded through a reduction of the
tolerance limit (Marras, 2006). When micro-damages occur, the tissue undergoes an inflammatory
process necessary to initiate a healing process and biological adaptation. If the natural cycle of
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