Acetabular Rim Damage

Etiology

The term acetabular rim syndrome was described as a pathologic condition wherein intrinsically normal intraarticular soft tissue structures were exposed to loading joint forces that physically exceeded their tolerance level, resulting in hip damage. The frequently enlarged acetabular labrum in dysplastic hips initially aids in maintaining the femoral head within the joint; however, the unstable femoral head potentially translates and eventually subluxes secondary to deficient coverage. If these chronic “inside-out” shear stresses do persist, labral soft tissue compensation will fail and the labrum can tear off the acetabular rim or can avulse with an osseous fragment. This is described as rim fracture.

Although management of damage/degeneration to the acetabular rim is still evolving, consistency in the location of damage within the acetabular rim has been demonstrated in several studies, both cadaveric and in vivo. Peripheral damage to the hip joint was first highlighted in the classic studies of osteoarthrosis conducted by Harrison and colleagues and Byers and coworkers. This was further supported by the work of Bullough and Goodfellow, who emphasized the importance of the shape of the hip joint in the form of minor incongruencies leading to failure of articular cartilage at the acetabular rim within normal daily contact. Despite these early reports documenting the acetabular rim as an early site of hip damage, specific disorders—such as hip instability due to dysplasia ( Fig. 35.1 ) and, more recently, femoroacetabular impingement (FAI; Fig. 35.2 ) were underappreciated as causative factors for hip osteoarthritis (OA). The acetabular labrum and adjacent cartilage are early structures to fail in acetabular rim disorders secondary to localized stresses. This notion was confirmed by Leunig and colleagues, who compared cadaveric findings and noted anterior acetabular quadrant damage with associated insufficient femoral head-neck offset. Seldes and coworkers further characterized acetabular rim damage as 2 main types of rim degeneration correlating with our current understanding of FAI.

In FAI, the femoral head is well centered, but the free arc of hip motion is either limited by the socket, producing pincer FAI, or a misshapen proximal femur, causing cam FAI, leading each alone or in combination to a mechanical conflict in which the articular damage is initially located within the acetabular rim. The site of hip damage is similar to that seen in hip dysplasia; however, failure mechanisms are almost the opposite. Furthermore, damage patterns of pincer and cam FAI differ substantially when one of these 2 types exists as an isolated deformity. In pincer FAI, pathology is more localized to the labrum; in cam FAI, damage takes place at the cartilage with “outside-in” abrasion and/or delamination, with the occasional rim fracture. An osseous rim fragment in FAI may be seen in athletes with a combined type and pronounced acetabular malorientation. Speed, force, and degree of hip motion, in addition to the quality of tissue at the chondrolabral junction, might contribute to enhanced vulnerability at the anterosuperior rim.

To date, our knowledge indicates that hip dysplasia and FAI are the two major bony deformities associated with the development of osteoarthritis in the hip. Alterations in hip joint mechanics represent a continuum between “undercoverage” (dysplasia) as described by Klaue and associates and, as introduced more recently, “overcoverage” (FAI). Despite the etiopathogenesis of the rim fracture , whether it is an unfused secondary ossification center or a stress fracture of the acetabular rim, preliminary reports on its surgical stabilization have shown postoperative improvement in pain and function. In addition, reports on iatrogenic hip instability after an arthroscopic rim resection have emphasized the importance of maintaining adequate acetabular bony coverage and a stable soft tissue envelope.

Acetabular Rim Damage and the Labrum

The acetabular labrum is triangular in cross-section, with the base applied to the acetabular rim and the apex being the free margin. The joint capsule attaches to its external edge, creating a potential recess between the capsule and the labrum. The labrum can be subdivided into 2 distinct zones: the extraarticular side, consisting of dense connective tissue, is well vascularized at its junction with the joint capsule; the intraarticular portion is largely avascular. Embryologic studies also showed differences with respect to the morphology and vascularity of the anterior and posterior part of the labrum and chondrolabral junction. In a study of 11 human embryos, Cashin and associates found that the orientation of collagen fibers within the transition zone differed depending on their location: posteriorly, the collagen fibers attached perpendicularly; anteriorly, the collagen fibers were parallel to the rim, making the labrum particularly vulnerable to shear forces and corresponding, to some extent, to the so-called watershed lesion . Based on intraoperative observations of a large number of hip arthroscopies for labral tears as well as cadaveric dissections, McCarthy and associates described the anterior labrum as an at-risk zone because of potentially inferior mechanical properties, higher mechanical demands, and relative hypovascularity. They proposed that a labral tear alters the biomechanical environment of the hip, leading to degeneration of the articular cartilage and eventual osteoarthritis. In contrast to this evidence, an anatomic study performed by Masłoń and colleagues revealed that there was a greater blood supply in the posterosuperior and anterosuperior quadrant of the acetabulum during fetal development.

In terms of its predilection for failure, Dorrell and Catterall correlated the occurrence of a labral tear with abnormal shear stresses transmitted by the uncovered femoral head, as may occur in acetabular dysplasia, which has also been a condition proven to increase the load supported by the labrum, ranging from 1% to 2% in a normal hip to 4% to 11% in a dysplastic hip. In this clinical situation, they postulated that the enlarged labrum contributes to stability of the femoral head within the acetabulum. Far from the initial idea of sharing a significant part of the joint load, Ferguson and colleagues found that the labrum mainly acts as a seal, ensuring more constant fluid film lubrication within the hip and limiting the rate of fluid expression from the articular cartilage layers of the joint, as noted by greater hydrostatic fluid pressurization within the intraarticular space with an intact labrum. As studied by Dwyer and associates in a cadaveric model, the sealing capacity is strongly affected by the position of the joint, indicating that activities that place the hip in repetitive flexion and internal rotation may increase the risk of degeneration because of the loss of fluid transfer under loading. In addition, because the labrum adds extra resistance to the flow path for interstitial fluid expression, cartilage consolidation has been shown to be significantly quicker without the labrum. Consequently, disruption of the labral seal could be detrimental to the overall nutrition of the cartilage, leading to its premature degeneration. Crawford and associates, after a study on nondysplastic hip specimens, reported that loss of the labral seal is the critical event leading to destabilization of the hip, shifting the hip center of rotation and making the hip susceptible to increased impact loading and repetitive trauma. These excessive loads were also demonstrated in finite element modeling, in which Henak and colleagues showed that the labrum in dysplastic hips carried 2.8 to 4 times the load, whereas the cartilage stresses did not differ significantly between normal and dysplastic hips.

It is interesting to note that the morphologic appearance of the labrum can differ on the basis of its underlying mechanism of failure: dysplasia or FAI. Klaue and colleagues and Leunig and coworkers showed that in dysplasia, the labrum is distinctly hypertrophic, with myxoid degeneration and/or detachment from the bony rim, whereas in FAI, the labrum is more commonly characterized by an undersurface tear with no hypertrophy. These findings can be helpful in establishing the dominating underlying bony abnormality when in the presence of mixed deformities such as dysplasia and FAI. In terms of pincer-type FAI, Seldes and associates described labral damage extending perpendicular to the surface of the labrum. In more severe cases, the damage reached the subchondral bone, with associated endochondral ossification of the labrum. With respect to cam-type FAI, these authors described a specific injury to the transition zone between the fibrocartilaginous labrum and the acetabular cartilage perpendicular to the articular surface, leading to a chondrolabral disruption.