Outline View

SIJ Degeneration

All normal synovial joint surfaces are smooth to promote gliding, but may become rough after injury in which the ligaments are sprained and stretched. As a result, the normal movement pattern changes. The joint surfaces rub at irregular angles, leading to wear and tear on the joint surfaces, which lead to degenerative changes such as roughenings, erosions, fibrotic changes, loose connective tissue strands and other amorphous cellular debris. Taken together, these changes are known as osteoarthritis.

Unfortunately, a misconception is promoted in the manual medicine field, called the keystone concept of form and force closure, which asserts that these changes are normal in one, and only one, particular joint, the sacroiliac joint. A fundamental principle of the keystone concept is that roughening and interlocking ridges and grooves that occur on the articular surfaces of the sacroiliac joint [1, 2] are considered normal developments in the adult, as a means of increasing friction to counter increased weight bearing during the aging process [3, 4]. For more, please see Keystone vs. Suspension.

However, according to the concept in which the sacrum is suspended from the ilia, as explained in Tensegrity, the sacroiliac surfaces do not touch during normal movement. Instead, the sacrum is pulled through its range of motion by ligaments and muscles. But, it is not unusual for ligaments to fail during traumatic events such as jumping, falling, or lifting heavy weight, or from chronic repetitive motions. In those situations, the joint surfaces may impact each other and rub. To minimize damage, the sacroiliac joint has developed a mechanism that protects itself from the deleterious effects of friction, as well as possible.  

The Nutation Lesion
It is known in metallurgy that, to minimize friction, one surface should be denser and harder than the other surface. The harder surface would slide easier on the compliant softer surface. If both surfaces were of equal hardness, they would create significantly greater friction. It is possible that an analogy exists in the sacroiliac joint, where the sacral hyaline cartilage surface is harder, and the softer iliac fibrocartilage surface exhibits greater degenerative changes.

In fact, Bowen & Cassidy [2] found that “the iliac cartilage surface is fibrocartilaginous, while the sacral surface is hyaline cartilage. Degenerative arthrosis of the joint commences at an early age, affecting the iliac cartilage to a greater extent than its sacral counterpart…whatever stresses the joint is subjected to, it would seem that the sacral hyaline cartilage has a better capacity to resist degenerative changes than the iliac fibrocartilage.” They found that, with increasing age, the surfaces of both sides of the sacroiliac joint degenerate and become irregular, leading to inter-articular fibrous adhesions, further limiting motion. However, they also stated that “the iliac cartilage exhibited more advanced changes of cartilage degeneration, with the surface becoming irregular, fibrillated, and eroded. The cartilage began to diminish in thickness…the joint cavity began to fill with greater quantities of amorphous, cellular debris.”

If we add to this image the concept that the sacrum is suspended by ligaments, we can get a more complete picture. Using holographic analysis, Vukicevic et al. [5], found that in a properly functioning sacroiliac joint, the articular surfaces of the sacrum and ilium do not make tight contact, even with a wide variety of loads. This indirectly supports Levin’s wheel analogy related to tensegrity [6], which indicates that the ilia generate a pivoting, rotary-type motion in the sacrum by pulling it through its range of motion. See Sacral Movement Induced by Innominates.

Vukicevic et al. [5] also found that while removal of the sacrotuberous and/or sacrospinous ligaments did not significantly affect sacroiliac joint motion, removal of the interosseous ligaments had a profound effect. When the interosseous ligaments were removed, the sacrum fell inferiorly, fixed between the ilia, and nearly stopped movement. Similarly, Simonian [7] found that damage to the sacrospinous and sacrotuberous ligaments did not significantly affect SIJ motion, but damage to the interosseous ligament caused significant displacement, indicating that the interosseous ligament is the “single stabilizing structure of the sacroiliac joint.” Also, Dujardin [8] found that, although sectioning of the sacrotuberous and sacrospinous ligaments had little effect on  SIJ motion, sectioning of the anterior and interosseous ligaments caused displacements which increased the gap between the sacrum and ilium and caused the sacrum to drop farther anteriorly and inferiorly (into excess nutation).

A nutation lesion may cause the sacrum to drop and wedge into the ilia, but to a lesser degree than a complete tear, resulting in aberrant motion and rubbing rather than a near stoppage of movement. This may explain the mechanism of the iliac upslip lesion, which is described as a superior movement of the ilium relative to the sacrum [9]. I suggest that the upslip lesion is similar to a nutation lesion but the latter term is more descriptive of the underlying biomechanics and systemic effects. Motion will change from unrestricted in all directions, as in youth, to an aberrant pattern. The normally smooth, frictionless, sacroiliac motion produced by pulling of the ligaments will become irregular, generating compressive and shearing forces.

Progressions with Aging
In view of the above, the ideal surface shape of the normal adult articular region is flat, as it is in youth [2], not to transfer weight during compression, but so the sacral and iliac surfaces can move very close together, yet not rub. However, once the ligaments are torn, the close proximity of the sacrum and ilium moving so close to each other would cause them to rub at irregular angles, transmitting shear forces throughout the central portions of the articular surfaces, but especially at the periphery of the joint, where the greatest degenerative changes have been found [2].

By the early twenties, the iliac surface develops a ridge running down the middle of the two wings. At the same time, the sacral surface develops a corresponding groove into which the iliac ridge moves. Following the development of this ridge and groove, in a simplistic two-dimensional view, the sacroiliac joint appears to move in a rotary motion along this track. However, I suggest that the ridges and grooves, both macro and micro, may have no normal functional significance and, therefore, may be the result of dysfunction after injury. Accordingly, I suggest that the smooth flat SIJ surfaces, as seen in youth, are normal and, without trauma, would remain so throughout life. Please see Ridge and Groove Development.

Degenerative Changes: Osteoarthritis
As the sacroiliac lesion progresses into a pathological state, the aberrant motion may cause increased rubbing of the central portions of the surfaces in an irregular pattern. This surface rubbing, with poor lubrication due to synovial fluid leakage through capsular tears [10], may cause erosions and development of smaller ridges and grooves on the articular surfaces.

Since fibrocartilage receives its nutrition from the surrounding fluid, it needs the pumping mechanism of joint movement for development and maintenance [11].
However, in an unstable sacroiliac joint, the growth of the ridges and grooves, and other degenerative alterations, may cause changes in joint position and movement patterns which may reduce motion and, thereby, nutrition inflow and waste removal, decreasing the fibrocartilage’s ability to regenerate. This irregular rubbing may cause significant degenerative changes over the years, and develop into osteoarthritis.

Respiration alone, at about 14 breaths a minute, occurs about 20,000 times a day. Another mechanism, the cranio-sacral fluid pumping mechanism, is reported to move the sacroiliac joint about 9 times a minute for, possibly, an additional 13,000 movements per day. Walking provides an additional 2,000 movements that put significantly more stress into the sacroiliac joint than either of these other mechanisms, due to the increased load and range of motion occurring. But, to be conservative, it is reasonable to use the figure of 20,000 movements a day to account for the alternating sacroiliac joint movements between nutation and counternutation. Each movement stresses the damaged ligaments and joint surfaces and leads to further degeneration.

If contact between the joint surfaces is made only after tearing of the interosseous ligament, the pressure that forms the ridges and grooves must be pathological. The ridges and grooves are seen as evidence of degeneration, as is the presence of tears, erosions, fibrotic changes, loose connective tissue strands, and other amorphous cellular debris [1, 2].

With the axial sacroiliac joint serving as a pivot point, the aberrant motion would provide an alternately compressive, shearing, and rotary force to the structures on each side, specifically the articular and syndesmosis regions. The development of similar and extensive ridges and grooves on both of these areas supports this concept.

Analogous to the articular region, the syndesmosis region of the ilium has a convex surface, and the sacrum has a corresponding concavity with similar degenerative changes, such as ridges and depressions, but smaller and with less roughening, although extensive [12]. Like the articular region, the severity of the ridges and depressions were found to be age-related, being worse in the older specimens and present in 100% of those over 55 years of age. Unlike the articular region, the syndesmosis region demonstrated internal ossification, most markedly in the central region, effectively fusing the sacrum and ilium at that point. Ossification occurred in 60% of the specimens over 60 years of age.

Considering that the syndesmosis region is the attachment point of the interosseous and short posterior ligaments, from which the sacrum hangs, and the articular region defines the arc of sacroiliac movement, one expects to see less movement and less development of the ridge and groove at the syndesmosis than at the articular region. With greater motion in the articular region, one would expect a larger ridge and groove, which has been observed [12]. With less motion and a primary function of support, fusion should occur more easily and be more necessary at the syndesmosis than in the articular region, which is what has been observed [12].

It follows that, if contact between the joint surfaces is made only after tearing of the interosseous ligament, then the pressure that forms all of the ridges and grooves, the large central one and all the smaller surface ones, must be pathological. The ridges and grooves themselves are seen as evidence of degeneration, as part of a disorder that includes the presence of tears, erosions, fibrotic changes, loose connective tissue strands and other amorphous cellular debris [1, 2].

Sashin [1] did a study of 257 cadavers divided into three groups, defined by age: Group I, 1 to 39; Group II, 30 to 50; Group III, 60 and above. In Group I, it was found that the sacroiliac joints were smooth and regular, except for two that showed microscopic degenerative changes. The joint space was narrow, and the surfaces were moist, with no free synovial fluid, except in two pregnant women. Pathologic changes were not evident. Group II developed irregular, uneven, and coarse granular tissue on the joint surfaces, mainly on the ilium. The sacral articular surface changed from a clear, cream-white color to a yellow hue. The iliac articular surface cartilage became irregular and coarsely granular, with erosions and osteophytes at the margins. Tears, erosions, and fibrotic changes, along with loose connective tissue strands appeared between the sacral and iliac surfaces. Blood vessels swelled within the joints and brought plasma cells and lymphocytes, sometimes replacing degenerated joint surface areas with vascular connective tissue. These changes appeared more as the subjects advanced from their 40s to their 50s, until mobility becomes very restricted and, in some cases, absent due to fibrous and boney ankylosis. Pathological degenerative changes were seen in 91% of males and 77% of females in group II. Group III showed degenerative changes in all SI joints with boney ankylosis present in 82% of the males and 30% of the females. Joint changes from group I to III were considered to be degenerative. Sashin concluded that “pathologic changes in the sacro-iliac joints are very common. These changes are progressive and increase both in extent and intensity with the age of the individual.”

Bowen & Cassidy [2] agree with Sashin but make two additional statements that should be noted. In childhood, the articular region of the sacroiliac joint is smooth and flat, with free movement in all directions [2]. By the early twenties, the joint surfaces begin to change; a convex ridge and a corresponding sacral groove develop along the length of articular surfaces. Further, they found that, in subjects over 30, “Plaque formation and peripheral erosions became increasingly common. The joint space contained some flaky, yellow, amorphous debris. By the 50s, “the articular surfaces became totally irregular with deep erosions, sometimes exposing the subchondral bone. A large amount of flaky, amorphous, yellow debris-covered both sides of the joint…” By the 60s cellular debris was common, and evidence of intra-articular fibrous interconnections or adhesions was observed. In later years, ankylosis within the joint is almost always due to fibrous adhesions whereas the boney ankylosis is more specifically said to be outside the joint, along the margins of the capsule. Only one joint, other than those with ankylosing spondylitis, had true boney ankylosis within the joint. In agreement with Sashin, the changes of the joint surfaces from smooth to rough with aging were considered to be degenerative, but they added that the degeneration occurred mainly at the margins of the joints.

Conversely, proponents of the keystone concept [3, 13-15] [4]p55 believe that the increasing roughening of the sacroiliac joint surfaces is a normal response to gains in body weight after puberty, which serves to increase friction as a functional adaptation to standing upright. They stated that this friction would, hypothetically, enhance form closure, and be beneficial in weight transfer during lifting, gait, and shock absorption. They considered these roughening to be “a nonpathologic adaptation to the forces exerted at the SI joints, leading to increased stability;” this is a central concept in the keystone form and function hypothesis. They dismiss pathology as a factor in joint surface changes and consider Sashin’s [1] and Bowen & Cassidy’s [2] conclusions to be merely opinions. However, a careful reading of their own study [3], will show that they picked out the parts of Sashin’s and Bowen & Cassidy’s studies that support their ideas and ignore the important parts that contradict them.

Vleeming’s and Snijders’ own studies only mention the beginning stages of degeneration, such as coarseness of the joint surfaces with interdigitating ridges and grooves, but make no mention of the signs of continued degeneration within the joint which would not agree with the concept of form closure, such as tears, erosions, fibrotic changes, loose connective tissue strands, and debris, as noted by other researchers. They refer to these signs of severe degeneration as simply “cartilage changes” or roughening. What they fail to consider is that, in any other joint or biomechanical model, these signs would signify moderate to severe osteoarthritis, and cannot be considered normal.

To supposedly test their concept, Vleeming et al. [13] studied the coefficients of friction of sacroiliac joint surfaces and found that roughening of the surfaces, and the presence of ridges and grooves, increased friction in the joint. While there is no doubt that friction was increased, it was misleading to saying that the friction in the sacroiliac joint was a normal response in a normal joint because any hypermobile joint will undergo shearing forces that degenerate the surfaces and limit motion.

Although it is evident that the roughening and development of small ridges and grooves increase friction and contribute to stability, these developments can only occur after the ligaments, particularly the interosseous ligament, tear, and motion becomes erratic, causing the joint surfaces to start rubbing. It is the rubbing that creates shearing forces that lead to degenerative surface changes. As in all synovial joints, roughening of articular cartilage, indicating wear and tear, are pathognomonic for degenerative disease.

Highly mobile, cartilage covered, non-suspensory weight-bearing joints, including the knee and ankle[16-18], do not exhibit the severe degeneration, such as interlocking ridges and grooves, which are evident in the sacroiliac joint; in other words, these other joints, when normal, have mechanisms to withstand weight-bearing without forming frictional surfaces. It is only after an injury to the ligaments that these joints undergo degenerative changes, which may loosely be interpreted as frictional surfaces.

Additionally, degenerative changes at the margins of other weight-bearing joints, such as the lumbar spine, including lipping and spurring, contribute to stability in hypermobile intervertebral joints, but there is no question that they are pathological. Yet, keystone proponents insist that similar changes in the sacroiliac joints are normal; otherwise, their model of form closure would fall apart.

On the other hand, although they did not doubt their contribution to stability in a dysfunctional joint, Sashin [1] and Bowen & Cassidy [2] considered these changes degenerative. Accordingly, Sashin [1] stated that “…the degenerative changes of the articular cartilage precede the osteo-arthritic changes about the joint. It seems clear that the osteophytic formations follow degeneration patterns of cartilage. This is the prevailing opinion among pathologists and was discussed in a paper on spondylitis deformans.”

Proposed Ridge and Groove Development
From the side, in a 2-dimensional perspective, the sacroiliac articulation appears to be shaped like an “L” with a vertical and horizontal portion. Each portion has an interlocking ridge on the ilium and corresponding groove on the sacrum. It has been thought that the interlocking ridge and groove guide the movement pattern of the sacroiliac joint [19] [20]p64-66 [14] [21]p49-51 but I suggest that the ridge and groove are more the results of the aberrant movement pattern imposed on the sacrum and ilia during gait and other activities. It is possible that the development of the large central iliac ridge and sacral groove, in addition to the smaller surface ridges and grooves, may be the result of degenerative changes after an injury to the sacroiliac ligaments.

Although the propeller shape of the joint surfaces complicates visualization of the movement patterns, a simple comparison may be made to a spinning plate coming to rest on a table. In this instance, induced by gait and other movements, I suggest that the sacrum wobbles against the ilia during nutation and counternutation movements, which allows compression to occur mainly at the perimeter of the joint. Shearing forces, introduced during sudden lifting or impact, may cause rubbing of the central portions of the joint.

Studies suggest that the combination of compressive and rotary forces, creating large shearing forces, can significantly induce metaplasia of fibrous tissue into fibrocartilage, forming sizeable fibrocartilaginous masses [11, 22, 23]. Bowen & Cassidy [2] stated that an increasing amount of collagen is laid down on both the sacral and iliac side as one age, but more so on the iliac side. I propose that it is possible for the fibrocartilaginous matrix on the iliac side, imbued with collagen fibers and stimulated by irregular compressive, rotary, and shearing forces, to swell and grow enough to fill in the central space, forming the iliac ridge.

As the sacroiliac injury progresses into a pathological state, the aberrant motion may cause rubbing of the central portions of the surfaces in an irregular pattern. This surface rubbing, with poor lubrication due to synovial fluid leakage through capsular tears [10], may cause erosions and development of smaller ridges and grooves on the joint surfaces.

Since fibrocartilage receives its nutrition from the surrounding fluid, not through vascularity, it needs the pumping mechanism of joint movement for development and maintenance [11]. However, in an unstable joint due to ligament laxity, the growth of the ridge and groove causes changes in joint position and movement patterns which may reduce motion and, thereby, nutrition and waste removal, decreasing its ability to regenerate. This irregular rubbing may cause significant degenerative changes over the years, including surface roughening, erosions, and amorphous debris. Because each person’s gait patterns are different, no two sacroiliac joint surfaces are alike.

Sacral Groove
In explaining the development of the sacral groove, I am the least sure of my ideas than anywhere else in my theory, but I offer two possible scenarios, either one or both together, may be true. However, I have little doubt that, through some mechanism, the iliac ridge and sacral groove are the results of degenerative forces.

1) The development of the sacral groove may be due to the occurrence of negative pressure changes of the surface on the sacrum. It may be that the combination of iliac fibrocartilaginous growth and sacral yielding creates the iliac ridge and sacral groove, similar to bone remodeling in tooth movement. As the cartilage on the iliac side grows, a remodeling effect may be created on the sacral bone matrix as it yields to the mechanical pressure and other physicochemical effects induced by the increased pressure of the growing cartilage against the reduced pressure within the sacral matrix.

2) At the periphery of the articular region, the softer iliac side may yield to the harder sacral side, as the compressive forces overcome the ability of the fibrocartilage to regenerate. Over time, the periphery on the sacral side may grow as the iliac side recedes; in this scenario, the central sacral surface does not necessarily recede because the growth at the edges may create the appearance of a groove in the center. It may be that the combination of central fibrocartilaginous growth and peripheral fibrocartilage yielding creates the iliac ridge and sacral groove.

With motion restricted by surface grooves and ridges and fibrous adhesions, the ability to induce motion in the sacrum is also reduced, resulting in less sacroiliac motion during gait. Shock absorption would also be reduced. I suggest that an affected person’s gait should shift from anterior-posterior to include more side-to-side movement, in concert with the significantly altered sacroiliac motion, as is evident in our older population.

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  15. Snijders, C.J., Transfer of Lumbosacral Load to Iliac Bones and Legs: Part 2 – Loading of the Sacroiliac Joints when Lifting in a Stooped Position. Clinical Biomechanics, 1993b. 8: p. 295-301.
  16. Anderson, D.D., et al., Intra-articular contact stress distributions at the ankle throughout stance phase-patient-specific finite element analysis as a metric of degeneration propensity. Biomechanics and modeling in mechanobiology, 2006. 5(2-3): p. 82-9.
  17. Anderson, D.D., et al., Physical validation of a patient-specific contact finite element model of the ankle. Journal of Biomechanics, 2007. 40(8): p. 1662-9.
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  23. O’Conor, C.J., N. Case, and F. Guilak, Mechanical regulation of chondrogenesis. Stem Cell Res Ther, 2013. 4(4): p. 61.
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