Cumulative Spine Loading - Fundamentals and Assessment Tools for Occupational Ergonomics - page 306

turnover of the intervertebral disc has been shown to take 500 days in a canine model (Urban et al., 1978)
and collagen production is thought to take even longer (Adams and Hutton, 1982; Porter et al., 1989).
This is supported in an in situ animal study using rats that revealed that intervertebral disc annular
damage was still present after a month of recovery (Lotz et al., 1998). Clearly once an injury is initiated
in the spine, cumulative loading has the potential to outpace the repair mechanism. This pathway
is further compounded by the lack of pain sensing fibers in the interior of the intervertebral disc.
Only the outer third of the annulus is innervated with pain sensing fibers (Bogduk, 1983; Cavanaugh
et al., 1995), so an injury can progress from the interior margin to the exterior boundary before there
is the potential for direct pain generation. The mechanical changes in this process are not well under-
stood and secondary pathways for pain generation could occur due to disc height change or altered
mechanics.

13.4 In Vitro Cumulative Loading Response and

Tolerance Limits

Historically the investigation into tissue tolerance has mainly focused on single-cycle destructive com-
pressive testing of spinal motion segments in vitro. While it is acknowledged that compressive tolerance
values can be modified by factors such as load rate, gender and age a single tolerance has been adopted for
acute compressive loading (i.e., 3400N [NIOSH, 1981; Waters et al., 1993]). While there has been a rela-
tive scarcity of repetitive in vitro spine tissue testing, it has been examined by researchers as early as the
1950s (Hardy et al., 1958). In the 1980s it was demonstrated that in vitro repetitive compressive loading
can generate spine injuries at sub-maximal levels (Adams and Hutton, 1983; Liu et al., 1983). These
studies in conjunction with the isolated tissue-based evidence presented earlier in this chapter form a
biomechanical basis for a sub-maximal spinal injury pathway.
Examination of the influence of load magnitude on cycles to failure was examined in work by Hansson
et al. (1987) and Brinckmann et al. (1988) using repetitive in vitro compressive testing. When the data
from both of these studies were examined (Figure 13.5) a nonlinear relationship between the magnitude
of loading and cycles to failure was evident (Callaghan, 2002). The curve fits for this data are relatively
weak (r 2 0.27), explaining a relatively small amount of the variance. However, they clearly indi-

cate a nonlinear trend (linear curve fit coefficients of determination values were 0.08 to 0.12) with loading
at a higher percentage of maximum strength having greater risk of injury with fewer loading cycles. The
variability associated with the human spine specimens used in both these studies introduces a great deal
of scatter caused by the lack of experimental control over factors such as age, prior loading exposure,
activity level, etc. Both of these studies examined loads that were in the upper range of loads that
workers would experience in a repetitive lifting scenario. The majority of specimens that failed within
these two in vitro experimental paradigms were tested above 60% of maximum strength (Brinckmann
et al., 1988; Hansson et al., 1987). The difficulty of testing in vitro specimens at lower magnitudes of com-
pressive loading is that a longer testing period is required, making the results questionable due to the
absence of biological processes and repair mechanisms that occur in vivo. In fact it has been hypothesized
that for lumbar vertebrae the endurance limit is 30% of maximum load (Brinckmann et al., 1988). This
suggests that below this value the body's ability for self-repair will be able to keep any micro-damage in
check for the majority of loading scenarios.
While there is clearly a direct relationship between the number of loading cycles applied to an in vitro
test specimen and the cumulative loading exposure it sustains, to date there has been no published work,
which has studied in vitro cumulative loading and injury mechanisms. An examination of the data of
Brinckmann et al. (1988) revealed a linear relationship between the number of loading cycles and the
cumulative loading sustained to failure, see Figure 13.6. (Callaghan, 2002). While it is intuitive that
an increased number of cycles will increase the cumulative loading, it highlights the fact that in vitro
specimens failed at varying levels of cumulative compression. In other words, there was no single
exposure value linking in vitro cumulative compression exposure and injury. The basic tissue evidence

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