The only dependent variable that was significantly affected by experimental condition over time was participant-perceived pain (Figure 1
001). Participant-perceived pain immediately following the hypertonic saline injection was significantly greater than prior to the hypertonic saline injection; this increase lasted until 10 minutes after the walking and injection trials were completed (P
001; Figure 1
). Means and standard deviations for the mechanical variables are presented in the Table.
None of the mechanical variables were significantly affected by experimental condition or time.
445) and medial–lateral (P
= .697) COP velocity during quiet-leg stance did not change between experimental conditions or across times.
= .960), medial–lateral (P
816), and vertical (P
= .899) time to stabilization during the landing task were not affected by experimental condition or time.
Similarly, medial–lateral COP position for every percentage of the stance phase of walking was not significantly influenced by experimental condition or time (Figure 3
The purpose of this study was to evaluate the independent effects of anterior knee pain on static and dynamic postural control using an experimental anterior knee pain model. Although the current model effectively produced anterior knee pain, the experimental anterior knee pain did not affect any of the mechanical measures related to quiet standing, landing, or walking. The authors believe that the results indicate that anterior knee pain does not independently influence static or dynamic postural control.
Using a single 0.75-mL hypertonic saline injection, the experimental pain model effectively caused anterior knee pain.
The participants reported an average peak pain level of 2.
9 cm on a 10-cm visual analog scale, with 10 being the highest score.
Also, all participants were pain free within 20 minutes after the injection.
Single injections of 0.25 mL,3,12,18,39
and 1.0 mL44
of hypertonic saline have also previously been used to induce experimental knee pain.
Bennell et al39
and Hodges et al12
used single injections of 0.
25 mL hypertonic saline solution to induce experimental anterior knee pain and reported that pain level peaked 2 to 3 minutes after the injection.
The current data are comparable to previously reported experimentally induced anterior knee pain levels43,44
6 and 3.2 cm on a 10-cm visual analog scale, with 10 being the highest score.
Furthermore, Henriksen et al43
reported that this pain level altered walking mechanics, indicating that the pain level in the current study should have been great enough to alter walking mechanics.
However, the current data were not as comparable to those reported by Bennell et al,18,39
who reported pain averages of 5.
8 and 6.2 using an 11-point numerical rating scale, with 11 being the highest score.
It is uncertain what is responsible for the differences in perceived pain levels in the aforementioned studies.
In addition to the visual analog scale used to quantify perceived pain, the current study could have been strengthened if a functional questionnaire and a perceived exertion questionnaire to further qualify effects of the experimental anterior knee pain had been included.
Increased COP velocity during single-leg quiet stance is believed to suggest decreased postural control,31
and we found that experimental anterior knee pain does not influence anterior–posterior or medial–lateral COP velocity during single-leg quiet stance.
Our COP velocity values were comparable to previously reported anterior–posterior (2.
02 ± 0.26 cm/s) and medial–lateral (1.84 ± 0.
17 cm/s) COP velocity values.45
Furthermore, our findings are somewhat consistent with a previous report that demonstrated that experimental knee pain does not influence bilateral COP in healthy older adults.18
However, in this previous report, the authors suggested that (1) COP was not influenced by pain because of compensation from the uninvolved leg and (2) pain does influence postural control; the current data do not support these ideas.
If experimental knee pain does influence postural control during quiet single-leg stance, then perhaps average anterior–posterior and medial–lateral COP velocity are not sensitive enough to reveal differences in static postural control due to the effects of pain.
Although perhaps not more sensitive, other relevant measures could have provided additional insight into this issue, including lower-extremity joint mechanics (kinematics and kinetics) and electromyography.
Increased time to stabilization during a landing task indicates stability,33
and the current data showed that experimental anterior knee pain does not influence dynamic postural control.
The authors believe that they are the first to use time to stabilization as a measure of dynamic postural control in an experimental knee pain model.
The time to stabilization values used in the current study are comparable to previously reported time to stabilization values (anterior–posterior = 1.
34 ± 0.16 seconds; medial–lateral = 2.
51 ± 0.93 seconds; vertical = 0.65 ± 0.24 seconds).33,46
Time to stabilization has been described as a sensitive and effective measurement of dynamic postural control for various samples,33,45,47
and we expect that time to stabilization was a valid method to measure effects of pain on dynamic postural control in the current context.
However, center of pressure position and velocity theoretically may not have reflected altered lower-extremity neuromuscular strategies resulting from knee pain, due to potential compensatory mechanics.
For example, it is possible that our participants modified hip and ankle mechanics in an attempt to compensate for altered knee mechanics.
These simultaneous mechanical alterations at multiple lower-extremity joints could theoretically mask one another and not be reflected in center of pressure measurements.
This idea could be relevant to the standing and walking tasks performed during this study.
Hip, knee, and ankle joint mechanics, as well as electromyography data, could elucidate this idea.
In support of this speculation, Henriksen et al43
showed that lower-extremity joint mechanics are altered as a result of experimental knee pain during walking.
Similarly, experimental anterior knee pain did not appear to affect dynamic postural control during walking, as measured by medial–lateral COP excursion during the stance phase of walking.
Henriksen et al43
observed a variety of mechanical alterations for the lower-extremity during walking while using the current pain model.43
The independent effects of anterior knee pain on postural control are difficult to study due to other confounding variables that are also related to knee joint pathology.
Consequently, an experimental pain model has been created to eliminate these confounding variables.
We believe that the current experimental pain model is a good representation of clinical anterior knee pain.
The infrapatellar fat pad contains nociceptors that are spread throughout the fat pad and facilitate fat pad sensitivity to pain.48
Also, nerve fibers in the infrapatellar fat pad contain substance P, a protein that triggers nociceptors, which is consistent with musculoskeletal nociception.27,28,39
When hypertonic saline solution is injected into the infrapatellar fat pad, substance P is released and chemically irritates the nociceptors.49
In addition, animal experiments have shown group III and IV nociceptive afferents are stimulated by hypertonic saline; this also indicates that the pathways elicited by the pain model are consistent with those of musculoskeletal pain.29,30
Although experimental pain may be similar to anterior knee pain and osteoarthritis pain, differences exist in the quality of pain.
Using this model, perceived pain exists for a relatively short duration (approximately 12 minutes in this study).
Perhaps, if pain had remained longer, changes in the center of pressure would have been observed.
Bennell et al18
hypothesized that the infrapatellar fat pad nociceptors may need longer stimulation to make changes to postural control.