Capsulotomy is necessary to navigate the joint for both diagnostic and therapeutic purposes. However, many authors now contend that iatrogenic instability may result if the capsulotomy is not closed (Fig. 1). As the number of hip arthroscopies has increased dramatically (up to 18-fold) over the past decade [1], warranted concern has been emphasized in the size and type of capsulotomy performed and its routine closure [2]. Capsular preservation (minimal capsulotomy, routine closure) is encouraged for the retention of normal anatomy and optimizing outcomes. The iliofemoral ligament is the strongest of four discrete hip capsular ligaments (in addition to ischiofemoral, pubofemoral, zona orbicularis), and its primary purpose is to restrain anterior translation, with hip extension and external rotation. This static soft tissue stabilizer of the hip joint is disrupted during interportal (anterolateral to mid-anterior; Fig. 2) and “T” (Fig. 3) capsulotomies. Three recent cadaveric biomechanical studies (Table 2) have illustrated the importance of the iliofemoral ligament to the structural integrity of normal hip joint mechanics: Iliofemoral sectioning results in increased external rotation, extension, and anterior translation with no difference between the intact and repaired state [3–5].

The ligamentum teres is a strong hip joint stabilizer (Table 3). It becomes taut with hip flexion, adduction, and external rotation. Despite its name “teres” (Latin for “round”), the ligament is actually triangular to flattened in shape for part of its intra-articular course (approximately 30–35 mm) [6]. Its diameter is highly variable and circumferentially covered with synovium. In the normal hip, the synovium is not highly vascular to the naked eye or with the arthroscope. However, in a hip with Legg-Calve-Perthes disease, the synovium and the ligament itself may be thicker with significant inflammation [7]. In a developmentally dysplastic hip, the ligament may be abnormally hypertrophic (thicker, longer) [7]. In traumatic ligamentum teres ruptures, the acetabular side tears before the femoral side and intra-substance tears are rare [8].

The ligamentum teres originates from the transverse acetabular ligament and spans the bony junction of the ischium-pubis from the 5 to 7 o’clock position on the acetabular clock face. It inserts on the femoral side at the anterosuperior aspect of the fovea capitis, which is a bare area without articular cartilage, located posteroinferiorly on the femoral head. Within the ligament is the artery of the ligamentum teres, a branch usually derived from the posterior division of the obturator artery and less commonly from the acetabular branch of the medial femoral circumflex artery (medial epiphyseal artery). Regardless of its source, the amount of vascularity supplied to the femoral epiphysis is variable and minimal.

The presence of microinstability does not preclude other concomitant intra- and extra-articular disorders. In fact, subtle instability may actually increase the stress response and potential damage to local structures including labrum, articular cartilage and underlying subchondral bone, ligamentum teres, iliopsoas tendon, iliotibial band, hip abductors, and the remaining normal capsule [9]. Further, FAI symptoms may be exacerbated due to the excessive motion [10]. Conversely, impingement may actually induce instability in the following four ways: (1) Excessive acetabular anteversion can result in anterior hip instability and posterior acetabular rim impingement; (2) excessive acetabular retroversion can result in anterior impingement and posterior instability; (3) excessive femoral anteversion can result in anterior hip instability and posterior acetabular rim impingement; (4) excessive femoral retroversion can result in anterior impingement and posterior instability. In a study that examined the association between arthroscopic iliopsoas tenotomy and femoral version, significantly worse outcomes were observed in subjects with greater degrees of femoral anteversion (>25°) due to the loss of the anterior dynamic stabilizing effect performed by the iliopsoas [11].

Cam impingement prohibits true ball-and-socket mechanics, thus causing anterior levering over the rim (fulcrum) with subsequent posterior instability [12]. With traumatic posterior hip dislocation, there is a greater prevalence of anterior cams and femoral retroversion than in normal hips [13]. In an exclusively athletic population with low-energy subluxation or dislocation and posterior acetabular rim fracture, cam and/or pincer impingement has been identified in 64–82 % of subjects [14–16]. In athletes with larger degrees of motion (such as ballet, dancing, gymnasts), there may be impingement-induced instability without abnormal cam or pincer deformities. In a cohort of 59 professional ballet dancers, only one hip had evidence of a cam deformity, while several other abnormalities were identified on magnetic resonance imaging due to a dynamic “pincer” mechanism from the extreme motion involved with their sport [17]. Further, while in the “splits” position, all hips subluxated (mean 2.1 mm). In comparison to a control group, the abnormalities in ballet included significantly more acetabular cartilage lesions (mostly superior), more labral tears (mostly posterosuperior to anterosuperior), and more superior herniation pits. Despite the latter study’s prevalence of imaging abnormalities, less than two-thirds of subjects were symptomatic at the time imaging was performed in a follow-up investigation [18]. Further, when examining certain ballet positions, the mean translation was up to 4.6 mm (6.4 mm in one subject) [19]. Whether or not the microinstability observed in these studies (with the associated intra-articular pathologies) will lead to early osteoarthritis is yet to be determined.

Discrete frank hip dislocation is at the end of the microinstability spectrum. In the postoperative setting, instability may occur along this spectrum to variable degrees. Nine cases of post-arthroscopic iatrogenic hip dislocation have been presented in the literature [10, 20–25]. Due to publication bias, this is likely a significant underestimate of the true incidence of instability following hip arthroscopy. Thus, many authors have subsequently recommended routine capsular closure during arthroscopy, which has both potential advantages and disadvantages (Table 4) [2]. The following patient-, hip-, and surgical technique-specific factors have been associated with this uncommon, but serious, complication: capsulotomy or capsulectomy without repair, labral resection (versus repair or refixation), aggressive acetabuloplasty rim trimming in dysplastic configurations, and overall capsular laxity [26]. In this situation, revision surgery (either arthroscopic or open) for capsulorrhaphy may be indicated.

In addition to the capsule, other structures may be pathologically involved in microinstability. Ligamentum teres ruptures may be a sign of microinstability, or they may cause microinstability. Two classification systems exist to categorize these injuries (Table 5) [27, 28]. The more recently defined classification, a descriptive classification, was published in a level IV evidence retrospective case series of 616 arthroscopies in which 51 % had ligamentum teres ruptures [28]. It was observed that patients with tears had significantly greater range of motion, less lateral acetabular coverage, larger labral tears, and more advanced acetabular articular cartilage damage [28, 29]. Despite the possible role that the ligamentum teres may play in hip stability, counter to this argument is that it is commonplace for the ligament to be resected during open surgical dislocation femoral osteochondroplasty without residual instability following surgery. However, close history and examination does reveal that these patients do have subtle instability, similar to that of a partial (Gray and Villar Type II) ligamentum rupture, rather than a complete (Type I) rupture [30]. In addition to the capsuloligamentous structures, the musculotendinous dynamic structures that cross the joint may be weak, potentially altering the axial/appendicular skeleton mechanics and leaving the joint less stable.