1 Acetabular Dysplasia 5 2 in the Reduced or Subluxated Hip 3 Jonathan G. Schoenecker, Ira Zaltz, Justin Roth, 4 and Perry L. Schoenecker 5 Introduction include: dysplasia, impingement and avascular 26 necrosis. The purpose of this chapter is to review 27 6 As first proposed by Dr. William Harris in the the pathologic processes of acetabular and proxi- 28 7 early 1980s, it has become clear that osteoarthri- mal femoral development that lead to acetabular 29 8 tis (OA) of the hip does not exist as a primary dysplasia in a located, or subluxated, hip. 30 9AU2 disease, or if it does, it is extraordinarily rare [1]. Emphasis will be placed upon understanding 31 10 The extensive experience in total hip replacement how the developmental milestones of the acetab- 32 11 surgeries over the last four decades have provided ulum influence the surgeon’s decision to operate, 33 12 extensive insight into the pathological hip joint and if so, whether to perform an acetabuloplasty, 34 13 processes that lead to hip OA [2]. In particular, redirectional, salvage or replacement procedure. 35 14 mechanical pathologies that cause damage to “Mechanical pathologies that cause dam- 36 15 either the labrum or the chondrolabral junction age to either the labrum or the chondro- 37 16 are often the initiating processes which instigate labral junction are often the initiating 38 17 acetabular and femoral head arthritis (Fig. 5.1) processes which instigate acetabular and 39 18 [3]. These key observations have stimulated the femoral head arthritis” 40 19 field of hip preservation, which focuses on deter- 20 mining the mechanisms that cause damage to 21 these structures and the development of surgical Pathophysiology 41 22 approaches that comprehensively correct these 23 pathomorphologies [4–8]. The three pathological Normal anatomical development of the hip 42 24 processes that lead to injury and degeneration of requires coordinated growth of both the acetab- 43 25 the labrum and the chondrolabral junction [1, 2] ulum and proximal femur that provides essential 44 femoral head coverage and clinical stability by 45 J. G. Schoenecker (*) the time the child is skeletally mature [9]. 46 AU1 Department of Orthopaedics, Vanderbilt University Normal acetabular development results in a con- 47 Medical Center, Nashville, TN, USA gruent hip joint with approximately 15° of ace- 48 e-mail: [email protected] tabular anteversion and sufficient coverage of 49 I. Zaltz the femoral head. At skeletal maturity, an intact 50 William Beaumont Hospital, Royal Oak, MI, USA hip joint is stable during weight bearing and 51 J. Roth · P. L. Schoenecker physiologic range of motion, without inappro- 52 Department of Orthopaedics, Washington University priate stresses on the chondrolabral junction. 53 Medical Center, St. Louis, MO, USA e-mail: [email protected]; Normal proximal femoral development results 54 [email protected] in a spherical ­femoral head with approximately 55 © Springer Nature Switzerland AG 2019 S. Alshryda et al. (eds.), The Pediatric and Adolescent Hip, https://doi.org/10.1007/978-3-030-12003-0_5 J. G. Schoenecker et al. a bc d Fig. 5.1 Prevailing theory of osteoarthritis of the hip. Years of improper loading of the hip results in tearing of Mechanical pathology leads to labral pathology and hip the labrum or the chondrolabral junction (yellow arrow). osteoarthritis. (a) Radiographs of a mildly dysplastic hip (d) Progression of the tear, or increased pathologic load- in 34-year old female with right hip pain (white arrow rep- ing leads to arthritis of the femoral head or the acetabulum resents position of patient chondrolabral junction). (b, c) (red arrow) 56 15° of femoral version and the tip of the greater motion and pain [10]. During ambulation, hip 87 57 trochanter at the level of the center of the femo- dysplasia may result in excessive stress on the 88 58 ral head. This normal hip development allows labrum and/or chondrolabral junction (Fig. 5.2), 89 59 for joint congruency during physiologic activi- abnormal abductor muscle tension (with gait dis- 90 60 ties, with physiologic motion of 90° of flexion, turbance), and malalignment of the limb leading 91 61 15° of internal rotation at 90° of flexion and a to distal joint pathologies. With these in mind, 92 62 90° arc of rotation with equal internal/external surgical approaches have been designed to pre- 93 63 rotation (45°) in the prone position. Proper fem- serve the hip joint, addressing the pathological 94 64 oral neck offset and alignment of the greater and mechanical problems presented by these pro- 95 65 lesser trochanters assures both normal muscle cesses. The goals of hip joint preservation sur- 96 66 tension and force vectors for hip rotation while gery is to restore stable acetabular coverage of 97 67 avoiding extracapsular impingement on the pel- the femoral head and achieve a near normal range 98 68 vis during physiologic joint motion. Adequate of motion, without femoral acetabular/pelvic 99 69 acetabular coverage, proper acetabular and impingement. Proximal femoral dysplasia may 100 70 proximal femoral version and 15° of external occur from primary developmental pathologies, 101 71 tibial torsion, results in a stable base to support such as proximal femoral focal deficiency, coxa 102 72 the torso over the limb with a foot-forward gait valga/vara or excessive version. It can also 103 73 during single leg stance. develop secondarily, from diseases such as Legg-­ 104 74 Hip dysplasia with a located, or subluxed, Calve-­Perthes disease, slipped capital femoral 105 75 femoroacetabular joint is associated with inap- epiphysis or avascular necrosis. These conditions 106 76 propriate development of either the acetabulum, are presented in detail in other chapters. 107 77 proximal femur or both. Either alone or in combi- Acetabular dysplasia may occur primarily from 108 78 nations, the resulting pathomorphologies cause failure of development or secondarily from 109 79 damage to the labrum/chondrolabral junction and improper loading by the proximal femur. The 110 80 articular cartilage, leading to premature degener- morphologic characteristics are dependent upon 111 81 ation of the hip joint [4–8]. Acetabular under-­ the stage of acetabular development at the time of 112 82 coverage of the femoral head produces instability insult. 113 83 of the femoroacetabular joint. In addition to dam- Acetabular development (Fig. 5.3) is a 114 84 aging intracapsular structures of the hip, intra- dynamic process of endochondral ossification 115 85 capsular/extracapsular impingement of the femur involving the cartilaginous anlage that includes 116 86 on the acetabulum or pelvis causes restricted two essential growth centers: the triradiate 117 5 Acetabular Dysplasia in the Reduced or Subluxated Hip ab cd Fig. 5.2 Micro-instability of the dysplastic hip damages micro-instability of the femoroacetabular joint during the chondrolabral junction. Hip dysplasia with a located, daily activities. (c) This instability ultimately leads to or subluxed, femoroacetabular joint refers to inappropri- damage of the (c) labrum/chondrolabral junction (red ate development of either the acetabulum, proximal femur arrow) or even (d) fracture of the acetabular epiphysis (red and or both. (a) Angle arrows represent insufficient lateral arrow). Ultimately, this damage leads to premature degen- center edge angle (LCEA) of the ossifying acetabular eration of the hip joint epiphysis. (b) The resulting pathomorphologies leads to 118 cartilage and the acetabular epiphysis (os acetab- response to the increased size of the femoral 148 AU3119 uli) [11–13]. During the first 4 years of life the epiphysis [12, 13]. 149 120 ­majority of acetabular development occurs via Acetabular dysplasia can therefore be broken 150 121 biomechanical molding, with sequential ossifica- down to three categories: (1) improper shape and/ 151 122 tion of the acetabular cartilaginous anlage and or delay in ossification of the cartilaginous anlage, 152 123 radial growth of the acetabulum (by the triradiate (2) damage to the triradiate cartilage, or (3) prob- 153 124 cartilage). The shape of the acetabular cartilagi- lems of shape and/or delayed ossification of the 154 125 nous anlage is primarily influenced through acetabular epiphysis. Problems of shape and/or 155 126 direct contact (articulation) with the femoral delay in ossification of the cartilaginous anlage 156 127 head. The femoral head must be stably reduced in occur early in life. As the cartilaginous anlage is 157 128 the true acetabulum for optimal acetabular growth considerably plastic, malformation most com- 158 129 and development. The cartilaginous anlage is monly occurs as a result of eccentric loading of the 159 130 considerably plastic during the cartilaginous proximal femur. This results in an altered hip cen- 160 131 phase and becomes much less plastic later on, ter which is typically superiorly migrated, 161 132 following vascular invasion and subsequent ossi- observed as a “break in Shelton’s line” on a weight 162 133 fication. The triradiate cartilage is responsible for bearing AP pelvis with femoral version neutral- 163 134 growth of acetabular width, which must match ized (Fig. 5.4). Severe subluxation may cause 164 135 the growth of the femoral epiphysis. In a normal more significant morphologic changes to the carti- 165 136 hip, the majority of the cartilaginous anlage has laginous anlage and resemble a dislocated hip on 166 137 ossified by 4 years of age [12, 13]. After 4 years radiographs. Additionally, inappropriate biome- 167 138 of age, triradiate cartilage growth continues to chanical loading may also delay the vascular inva- 168 139 widen the developing acetabulum to accommo- sion and ossification of the cartilaginous anlage 169 140 date a larger proximal femoral epiphysis [12, 13]. which is observed as an abnormal acetabular index 170 141 Triradiate cartilage growth is typically complete (AI) (Fig. 5.5).