Human subjects with LBP had, on average, 25% greater perimuscular connective tissue thickness and ultrasound echogenicity in the lumbar region than did subjects without LBP after adjusting for BMI. There was no significant correlation between ultrasound structure and age and no significant differences between men and women. Although we did find a positive correlation between connective tissue structural measures and BMI, this relationship did not explain the differences observed between LBP and No-LBP groups. Moreover, activity levels were similar in both groups suggesting that abnormal connective tissue structure was not due a more sedentary lifestyle in the LBP group.
We do not know, at this point, whether the observed increase in connective tissue thickness and echogenicity are part of the cause or the effect of low back pain. One possibility is that abnormal connective tissue structure (possibly genetically determined) predisposes to the development of chronic or recurrent LBP. Connective tissue also may have remodeled over time in responses to repetitive stresses created by pre-existing altered movement pattern secondary to repetitive motion, habitual postures or sports, with or without tissue injury that predated the onset of LBP [37
]. Once pain is present, connective tissue abnormalities may worsen as a result of altered movement patterns due to pain or fear of pain [28
]. This would be consistent with the observed positive correlation between connective tissue measurements and symptom duration. In other types of connective tissues (e.g., ligament, joint capsules) the combination of inflammation and reduced mobility can lead to debilitating tissue fibrosis, adhesions and contractures leading to further tissue stiffness and movement impairment [38
]. So far, however, a similar pathophysiological process involving non-articular connective tissues has not been studied in relation to LBP.
The absence of association between our ultrasound measurements and symptom severity could be due to the fact that pain and disability levels were, on average, quite low in our LBP population, which could have interfered with our ability to detect a correlation. The subjects with low back pain who volunteered for our study were generally active people who managed to live busy lives despite the presence of low back pain, and most of these subjects had mild or moderate levels of pain. Many subjects with and without low back pain practiced yoga or did stretching exercises regularly. Additionally, a number of people with more severe low back pain had to be excluded because of a history of either prior back surgery or corticosteroid injection. Therefore, given these factors, it is remarkable that we found substantial differences in connective tissue morphology between our groups despite the low level of pain in the low back pain group. We might have seen even greater differences between groups and a stronger association with symptoms had our subjects with LBP been more severely impaired and less physically active.
We have chosen not to use the terms "superficial fascia" and "deep fascia" in describing our findings because of frequent uncertainty in determining the anatomical boundary between these two structures in both live imaging and gross anatomical specimens. According to the traditional anatomical definition, the term "superficial fascia" refers to an enveloping layer directly beneath the skin formed by a fine three-dimensional meshwork containing loose areolar connective tissue and fat within its meshes, while the term "deep fascia" refers to a continuous layer of dense connective tissue that invests muscles and tendons [46
]. However, in many subjects we observed multiple echo-rich layers (containing mainly dense connective tissue) separated by echo-poor layers (containing mainly fat) from dermis to muscle, with no clear distinction between superficial and deep fascia (Figure ). In other subjects, only one thickened dense connective tissue layer appeared to be present overlying the muscle (Figure ). It is thus not clear whether connective tissue morphology such as that shown in Figure is due to the presence of multiple connective tissue layers within the superficial fascia or due to fatty infiltration and disorganization of the perimuscular layer. We believe that the greater average perimuscular connective tissue thickness and echogenicity in the LBP group likely reflects a combination of increased thickness and increased numbers of connective tissue layers in subjects with LBP.
Examples of ultrasound images illustrating thin (A), thick (B) and multilayered (C) perimuscular connective tissue morphology.
Although this has not yet been studied, an important function of loose connective tissue layers may be to allow dense connective tissue sheets to glide past one another. Increased thickness and disorganization of connective tissue layers due to inflammation, fatty infiltration, fibrosis and adhesions may impair the normal relative movement of connective tissue planes, increase tissue stiffness, decrease range of motion and predispose to further injury [28
]. Fatty infiltration and herniation through disorganized connective tissue layers may also cause pain due to trapping of sensory nerve fibers through the collagen matrix [17
In this, study, we chose to recruit subjects with chronic LBP of more than twelve months duration in order to maximize our chance of detecting any connective tissue abnormalities, since connective tissue remodeling and fibrosis are relatively slow biological processes that cause morphologically detectable changes over weeks to months, rather than hours to days. We cannot at this point generalize our conclusions to subjects who have had low back pain for less than twelve months. A future longitudinal study evaluating connective tissue in subjects presenting with their first episode of low back and following these subjects over time may shed some light on this issue.